Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5850_Библиотеки_им_академика_М_И_Перельмана
.pdf
Herbal Medicines fortheTreatment
https://t.me/medicina_free
ofCOPD
SamirRanjanPanda, SiddhiJain, N.P.Syamprasad,
PriyankaAdhikari, MeenakshiSingh, AlokRanjan,
A.Parthiban, andV.G.M.Naidu
Abstract
Numerous epidemiological studies have shown that chronic
obstructive pulmonary disease (COPD) can lead to the
development of lung cancer (COPD). The comorbidities
are frequently linked to exposure to cigarette smoke, and
patients with COPD have an eightfold increased risk of
lung cancer death. Lung cancer can start in individuals with
COPD due to the heterogeneous nature of the two conditions, which are dened by several sub- phenotypes brought
on by telomere shortening, mitochondrial malfunction,
hereditary susceptibility, failure in the body’s defense system, and DNA repair processes. Emphysema, persistent
inammation, chronic bronchitis, and asthmatic bronchitis
are frequently linked to COPD.Bronchodilators have been
recognized as an effective therapeutic technique in reducing the symptoms associated with COPD via the evolution
of research for more than 200 years. Finding medications
that reduce inammation and slow the course of COPD is
still a necessity. Several inammatory and chronic diseases
have been treated with herbal remedies and medications.
Samir Ranjan Panda and Siddhi Jain contributed equally to first
author.
S. R. Panda · S. Jain · N. P. Syamprasad
Department of Pharmacology and Toxicology, National Institute of
Pharmaceutical Education and Research (NIPER),
Guwahati, Assam, India
P. Adhikari · M. Singh · A. Ranjan · A. Parthiban
Center for GMP Extraction Facility (Department of
Biotechnology), National Institute of Pharmaceutical Education
and Research (NIPER), Guwahati, Assam, India
V. G. M. Naidu (*)
Department of Pharmacology and Toxicology, National Institute of
Pharmaceutical Education and Research (NIPER),
Guwahati, Assam, India
Center for GMP Extraction Facility (Department of
Biotechnology), National Institute of Pharmaceutical Education
and Research (NIPER), Guwahati, Assam, India
e-mail: vgmnaidu@niperguwahati.ac.in
Many herbal medications are used to treat chronic illnesses
like cancer, neurological diseases, and metabolic diseases.
Along with powerful therapeutic advancements in the isolation, extraction, and therapeutic efcacy of herbal medications, there are numerous reports of decreased side
effects and organ toxicity. Finding new and potent herbal
medications with fewer side effects has become increasingly important due to an alarming rise in morbidity and
mortality among COPD patients.
Keywords
COPD · Herbal medicines · Novel mechanism ·
Molecular targets
1 Introduction
Tobacco smoking dates back to its origin in the Mayan kingdom in 600–900 AD [1]. Shamanistic rituals all over the
Americas smoked tobacco and hallucinogenic drugs as early
as 5000 BC [2]. Tobacco smoking is a worldwide epidemic
and is the prime risk factor for chronic obstructive pulmonary disease (COPD), lung cancer, and heart disease. In the
US, COPD and lung cancer represent the second and fourth
leading causes of death, respectively [3]. According to the
WHO, it is estimated around 3.17 million deaths occurred
globally in 2015 (accounting for 5% of deaths globally in
that year) due to COPD, which is currently ranked as the
third leading cause of death in the world. The Global Burden
of Disease Study in 2016 reported two hundred fty-one million cases of COPD [4]. Evidence of airway obstruction with
a usual decline in the functional parameters of the lung leads
to aging and COPD.Progressive decline in lung function and
airway obstruction causes dyspnoea (shortness of breath)
and irreversible structural changes in the lung tissues [5].
Source contributing factors responsible for causing COPD
has been described in Fig.1.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. K. Dhara, S. C. Mandal (eds.), Role of Herbal Medicines, https://doi.org/10.1007/978-981-99-7703-1_9
167
168
https://t.me/medicina_free
S. R. Panda et al.
Fig. 1 Source contributing factors in causing COPD
The earliest description of COPD with the name “voluminous lungs” is given by Bonet in 1679, while Badham
described the clinical understanding of chronic bronchitis
and bronchiolitis of COPD in 1814. In 1846 with the invention of the spirometer by John Hutchinson, the diagnosis of
COPD became easy. Christie in 1944 gives a detailed
description of the individual component involved in COPD
based on past research and physical examination of the
patients. The physicians Barach and Beckerman 1956 wrote
the book Pulmonary emphysema with a detailed description
of the treatment of the disease; in this book, they also describe
the expiratory airway ow volume pattern in emphysema
and the use of the spirometry [6].
Herbal medicines have been used by an ancient civilization, and archaeological evidence dictates their use from the
Paleolithic age. Several herbs, such as mint, clove, roses, lilies, rosemary, sage, ephedra, and fennel, have been used for
their treatment against acute and chronic inammatory diseases [7].
2 Molecular Mechanisms Involved
inCOPD
COPD is characterized by various processes like chronic
bronchitis, emphysema, and airway remodeling, affecting
all lung parts, including small and large airways and parenchyma, which contribute to chronic airway obstruction.
Chronic bronchitis is a clinical feature due to a chronic
increase in bronchial secretions, characterized by productive cough with submucosal glandular hypertrophy and
hyperplasia, with dilated ducts in airways down to 2–4mm
in internal diameter. Emphysema is an anatomicopathological diagnosis dened by permanent destructive enlargement of airspaces distal to the terminal bronchioles,
contributing to airow limitation resulting from loss of
lung elastic recoil [8]. Other features contributing to COPD
are the progressive loss of the alveolar wall, vascular
remodeling with pulmonary hypertension, and peribronchiolar brosis [9].
Herbal Medicines fortheTreatment ofCOPD
https://t.me/medicina_free
169
2.1 Role ofInammation andOxidative
Stress
Earlier evidence conrms that biomass fuels, smoking, air
pollution, and industrial dust are the principal elements of
the environmental hazard causing COPD [10]. According to
the American Lung Association, cigarette smoke contains
several harmful constituents and is a well-recognized risk
factor for about 85–90% of all COPD cases [11]. Cigarette
smoke contains more than 10,000 compounds, mainly constituting nicotine and polyaromatic hydrocarbons [12]. On
its continuous exposure, it activates various immune cells
and airway epithelial cells by releasing various proinammatory cytokines. Cigarette smoke generates lots of
oxidative free radicals, which generate oxidative stress by
activating various inammatory pathways [13], as depicted
in Fig. 2. Chronic exposure to cigarette smoke releases a
greater amount of proinammatory cytokines and chemokines such as tumor necrosis factor-alpha (TNFα), interferongamma (IFNγ), interleukins, monocyte chemoattractant
protein-1 (MCP-1), matrix metalloproteinase-12 (MMP-12),
and macrophage inammatory protein-2 (MIP-2) by activating immune cells, alveolar macrophages, airway epithelial
cells, smooth muscle cells, and broblasts [14]. The underlying cellular and molecular mechanisms involved in the onset
of COPD and asthma are comparable at earlier stages. Even
though both diseases include inammation as a primary criterion for disease pathogenesis, the inammatory signaling
and therapeutic response patterns are subtler.
2.2 Role ofGrowth Factors
Previous studies put forward the role of growth factors like
transforming growth factor beta (TGFβ), epidermal growth
factor (EGF), broblast growth (FGF), platelet-derived
growth factor (PDGF), and vascular endothelial growth factor (VEGF) in airway tissue remodeling in COPD [15]. The
vascular and epithelial cells of COPD subjects showed
increased expression of FGF-1, FGF-2, and FGFR1 [16].
Earlier reports also suggest that FGF–FGFR axis plays a role
in tissue remodeling by increasing collagenase expression in
lung broblasts [17]. TGFβ is another crucial growth factor
involved in wound repair, overexpression of which results in
epithelial to mesenchymal transition (EMT) where activated
epithelial cells cause the formation of attened mesenchymal traits leading to peribronchiolar brosis of small airways
[18]. On the other hand, TGFβ also acts as chemotactic for
cytotoxic T cells, neutrophils, and macrophages and causes
activation of various proteases through EGFR [19] for release
of matrix metalloproteinase (MMP-9/12), neutrophil elastase resulting in alveolar wall destruction and enhanced
Fig. 2 Graphical representation of mechanism involved in initiation and progression of COPD
170
https://t.me/medicina_free
S. R. Panda et al.
mucous secretion from goblet cells of airway tract [20].
VEGF is a chief controller of vascular growth functions
involved in pulmonary vascular remodeling, which occurs
due to vasoconstriction and collapse of the pulmonary circulation in severe COPD [21]. VEGF has a diverse function in
chronic bronchitis and emphysema. Former evidence hypothesize the role of increased expression of VEGFR1in emphysema and VEGFR2in chronic bronchitis [22]. VEGF has a
higher afnity for VEGFR1 than VEGFR2, resulting in vascular endothelial cell apoptosis, higher production of MMP,
and alveolar and vascular destruction leading to emphysema
[23]. In contrast, VEGF has a higher afnity for VEGFR2
than VEGFR1, resulting in angiogenesis and vascular remodeling leading to chronic bronchitis [24]. Hence, balance
among VEGF, VEGFR1, and VEGFR2 is critical for airway
disease pathogenesis.
2.3 Role ofProteases
Proteases are set of enzymes involved in inammatory
responses via the breakdown of elastin, a connective tissue network in the lung parenchyma, thereby creating an imbalance
between endogenous antiproteases and proteases, leading to
the development of emphysema [25]. Long ago, it was proposed that neutrophil elastase (NE), besides having strong elastolytic activity, is a potent stimulator of the MUC5AC gene,
thereby resulting in excess mucus secretion in airway epithelial
cells [26]. There is increasing evidence for the role of antiproteases, namely, α1-antitrypsin (α1-AT), in early- onset emphy-
sema features [27]. α1-AT has a potent inhibitor of Proteinase
3, which is expressed on the surface of cytokine- activated neutrophils [28]. Inheritant deciency of α1-AT or its inactivation
by cigarette smoke exposure raised the possibility of emphysema development [29]. Several other cathepsins (lysosomal
cysteine proteases) also show elastolytic activity, and overexpression of IFN-γ by smooth muscle cells and alveolar macrophages markedly increase the expression of cathepsins in
emphysema subjects [30]. Most of the MMPs are involved in
disease pathogenesis, but MMP-12 is prominent in mice, and
MMP-9 is most important in humans [31]. The interest in the
role of MMPs has sharply increased in the pathogenesis of
emphysema and small airway brosis. Increased activity of
MMP-1 (collagenase) in BAL concentrates and type II pneumocytes, and MMP-9 (gelatinase B) in lung parenchyma of
emphysematous subjects produce chemotactic peptides which
encourage macrophage recruitment in airways [32]. In addition, MMP9 can convert latent form of TGFβ to its active form
by elastolysis resulting in small airway brosis [33].
2.4 Other Signaling Mechanisms Involved
The inammatory changes, oxidative stress, and protease
imbalance are equally responsible for impaired lung function
in both smoker and non-smoker COPD subjects. The
increased prole of lipid mediators like prostaglandins
(PGE2 and PGF2α) and leukotrienes (LTB4) were found in
sputum and exhaled breath condensates of COPD patients
[34]. Another central molecular mechanism involved in the
amplication of inammatory responses in COPD is due to
reduced HDAC activity in alveolar macrophages and peripheral lungs [35].
3 Novel Strategies andMolecular
Targets inCOPD
The current rst-line therapeutic drugs used in treating
COPD deliver bronchodilatory effects, providing only symptomatic relief, and ultimately were of no benet. However,
the underlying mechanism intricated in COPD is still not targeted due to reliance on reliever medication rather than preventer medication. Strong evidence exists for the orchestra
of inammatory response and oxidative stress in
COPD.Molecules inhibiting these responses can provide a
most promising approach to monitoring COPD.
3.1 Targeting NF-κB Inammatory
Signaling inObstructive Airway
Disease
NF-κB family is believed to play a cardinal role in diverse
acute and chronic inammatory diseases. In the last 20 years,
NF-κB signaling has gained the focus of extensive research
[36]. NF-κB is activated utilizing numerous stimuli, counting physical and chemical stress in multiple steps controlled
by diverse enzymatic signaling. Further, several markers of
activated NF-κB signaling were identied in sputum and
bronchial biopsies of COPD patients [37]. Eucalyptol [38],
Asiatic acid [39], Zanthoxylum bungeanum seed oil [40], and
Ivy (Hedera helix) leaf extract [41, 42] are a few of many
other plant extracts which showed anti-inammatory activity
against chronic obstructive disease via inhibiting
NF-κB.PM014 herbal formula, a mixture of seven spices,
exhibited more signicant anti-inammatory effects in a
COPD mice model [43, 44]. Thus, anti-inammatory molecules possessing NF-κB inhibitory activity can greatly promote lung repair.
Herbal Medicines fortheTreatment ofCOPD
https://t.me/medicina_free
171
3.2 Targeting NLRP3 Inammasome
Signaling inObstructive Airway
Disease
Recent evidence suggests the role of NLRP3 inammasome
and associated markers in airway inammation [45]. Firstly,
NLPR3 inammasome formation is triggered under stress
conditions owing to cellular and tissue damage by PAMPs,
DAMPs, and toxins [46]. Secondly, the active form of caspase- 1 is released in the process of inammasome formation,
which cleaves pro-IL-1β and pro-IL-18 further to orchestrate
the release of mature cytokines [47]. Therefore, manipulating the inammasome formation using NLRP3 inhibitors or
blocking selective caspase-1 inhibitors can mitigate airway
inammation in COPD subjects. Melatonin [48, 49],
(−)-Epicatechin [50], Silybin [51], Histidine [52], and
Magnesium isoglycyrrhizinate [53] are a few natural molecules displayed prominent NLPR3 inhibitory activity invitro
and invivo COPD models. Hibiscus noldeae Baker f. [54]
and Berberine [55] revealed signicant repressing effects on
caspase-1 activities, thereby overcoming inammation and
apoptosis of airway epithelial cells. Molecules with dual
NLRP3 and caspase-1 inhibitory activity could ultimately
benet managing COPD.
3.3 Targeting Cytokine Release
inObstructive Airway Disease
Mounting evidence conferred cytokines and chemokines’
involvement in airway inammation and remodeling, goblet
cell hyperplasia, mucus secretion, and pyroptosis [56].
Hence, inhibiting the release of cytokines could be a promising approach to underpin progressive inammation. Leaf
extracts of Azadirachta indica [57], Perilla frutescens [58],
and Eriobotrya japonica [59, 60] are a few examples of
herbal extracts suggesting their potent use in the treatment of
COPD via impeding the production of cytokines.
Accordingly, this class of drugs can represent a target for
novel therapies in COPD subjects.
3.4 Targeting Proteases inObstructive
Airway Disease
A line of recent studies believed that elastolytic proteases
released by immune cells trigger elastin and other ECM protein destruction in the alveolar lining [61]. Anti-proteases are
better therapeutic agents to block elastolytic activity. Serine
protease inhibitors block the activity of neutrophil elastases
and other serine proteases their reverse the impaired proteases and anti-proteases balance [62]. Circulating
α1-antitrypsin is an endogenous anti-protease in the human
body that blocks neutrophil elastase activity. Apocynin
improves emphysema in the hamster model by selectively
inhibiting NADPH oxidase and protecting the activity of
endogenously released secretory leukocyte protease inhibitor (a protease inhibitor) [63]. Anemoside B4, a bioactive
component of Pulsatilla chinensis, played a vital in restoring
the protease and anti-protease imbalance in the CS-induced
COPD murine model [64].
3.5 Targeting Kinases inObstructive
Airway Disease
Inammatory and oxidative stress signaling activates the
p38MAPK cascade [65]. The degree of activation of
p38MAPK is directly related to the severity of lung function
impairment and airway inammation [66]. The rst-line
therapeutic drug, inhaled corticosteroid, requires glucocorticoid receptor (GR) to mediate its anti-inammatory activity.
Glucocorticoid resistance in COPD subjects could be due to
the ability of p38MAPK to phosphorylate glucocorticoid
receptor (GR), thereby restricting nuclear translocation and
DNA binding of GR [67, 68]. On the other hand, phosphatidylinositol 3 kinase (PI3K) is a signicant controller of
diverse cellular functions, including proliferation, survival,
autophagy, metabolism, and angiogenesis [69]. Activated
PI3K phosphorylates phosphatidylinositol diphosphate to
phosphatidylinositol triphosphate, further activating protein
kinase B (AKT). Further, dysregulated PI3K/AKT signaling
is involved in immune cell activation, the release of inammatory mediators, airway remodeling, excess calcium
release, and bronchoconstriction [70]. Upregulated PI3K/
AKT signaling downregulates histone deacetylase HDAC2
resulting in glucocorticoid resistance [71]. Molecules targeting p38MAPK and PI3K/AKT signaling can be better therapeutic targets by impeding the inammatory processes and
overcoming glucocorticoid resistance. Bufei Huoxue capsule
[72], Silymarin [73], and Theaavin-3,3′-digallate [74]
attenuate cigarette smoke-induced COPD via suppressing
ERK/p38MAPK signaling in the invitro and invivo model.
Castanea crenata inner shell extract [75], Citrus grandis
exocarpium [76], and Glycyrrhizic acid [77] are examples
shown in the current review to have an inhibitory effect on
PI3K/AKT signaling to display potential benets against
cigarette smoke-induced emphysematous lesions in mice
model.
3.6 Targeting Phosphodiesterase
inObstructive Airway Disease
Cyclic adenosine monophosphate (cAMP) is a secondary
messenger vital in mitigating COPD’s two major patho-
172
https://t.me/medicina_free
S. R. Panda et al.
physiological factors. An elevated level of cAMP helps
relax the smooth muscle and abate inammation. cAMP is
regarded as a pompous target in treating chronic respiratory
inammatory obstructive disease [78]. Phosphodiesterases
(PDE) are a superfamily of enzymes that cyclic hydrolysis
nucleotides like cAMP and cGMP to their corresponding
inactive derivatives AMP and GMP and help in regulating
the intracellular levels of these cyclic nucleotides [79].
Altogether, PDE promotes bronchoconstriction by reducing
the cellular levels of functional cAMP and elevating intracellular calcium levels. Henceforth, molecules targeting
PDE enzyme or increasing cAMP levels can be benecial in
providing bronchorelaxation in COPD subjects. Commercial
Thymus vulgaris extracts increased cAMP levels and
reduced intracellular calcium levels in the reconstituted
invitro system of MucilAir 3D human COPD airway epithelium [80]. Pistacia weinmannifolia [81] and Psidium
guajava [82] showed PDE inhibitory activity in lung tissue.
Isoforskolin, an active component of Coleus forskohlii, is an
activator of adenylyl cyclase, thereby enhancing the cellular
levels of cAMP and mitigating Cigarette smoke-induced
COPD in a rat model [83].
3.7 Targeting Oxidative Stress
inObstructive Airway Disease
Similar to inammation, oxidative stress is a signicant factor in the pathogenesis and exacerbation of airway disease
inammation [84]. Oxidative stress is known to intensify
immune cell inltration into the lung, the terrible release of
pro-inammatory cytokines, and the apoptosis of alveolar
epithelium responsible for airway hyperresponsiveness and
alveolar obliteration [85]. Repair of impaired oxidant and
anti-oxidant mechanisms could mitigate oxidative stressinduced alveolar damage. Andrographolide [85],
Dihydroquercetin [86], Resveratrol [87], Oroxylin A [88],
Propolis [89], and Ursolic acid [90] promote lung repair via
restoring anti-oxidant capacity through activation of Nrf2
pathway in COPD murine model.
4 The Natural History ofHerbal
Medicine
Since ancient times, to cure diseases, human beings have
searched for practical solutions in Mother Nature and found
most of the remedies from the plant herbs abundant in
nature. In the beginning, the use of plant herbs was mainly
limited to animals as the knowledge about diseases and
plant herbs was limited, but gradually the use increased for
diseases related to human beings as the knowledge about
plant herbs increased [91]. Hence, herbal medicine has traveled a long route throughout the centuries in the form of the
knowledge and skills that pass through the different generations/civilizations in the families/society for treating diseases using the medicinal plant herbs surrounding us.
Traditionally, the treatment given by the use of herbal medicine is based on the holistic approach of focusing on the
health rather than the disease, so the treatment methods vary
according to the geographical location and environmental
conditions. Also, many written historical scripts describe
the use of medicinal plants for herbal medicine. For example, for details regarding Indian Vedic scripts, Pen T’Sao by
China Emperor Shen Nung, Ebers Papyrus by Georg Ebers,
and De Materia Medica by Dioscorides etc., refer Table1.
The oldest evidence about the plant herbs was found in the
Sumerian clay slab from Nagpur, and Dioscorides, known
as the father of pharmacognosy, wrote details about the
plant herb’s appearance, local name, collection processes,
location, herbal medicine preparation, and their therapeutic
effect [7, 92, 99].
Between the sixteenth and eighteenth centuries, compound drugs, which consist of plant herbs and drugs from
plants and animals, increased. So, by seeing the importance
of herbal medicine, Linnaeus, in 1707–1788, wrote a book
called Species Plantarum in which he described the classication of the species and coined the word genus for the
polynomial system. In the nineteenth century, the discovery
of alkaloids, glycosides, vitamins, hormones, etc., from the
plant poppy, quinine, and pomegranate, etc., initiated the
scientic pharmacy for herbal medicine. With the end of
the nineteenth and the start of the twentieth century, the
decline in trust for herbal medicine started due to shortcomings caused by the fundamental changes in the plant
herbs during the drying process. Another reason for the
decline of traditional medicine is the development and
mass production of chemically synthesized drugs, which
give a faster therapeutic effect than herbal medicine. So,
the stabilization method was developed to tackle the problem related to the imbalanced herbal medicine composition, which consists of the standardization of the cultivation
and manufacturing conditions. Also, the development of
the chemical and physiological studies for the numerous
plant herbs along with the clinical studies to create a database of the drug from the plant-based herbs. Currently,
pharmacopeias like the United State Pharmacopoeia XXXI,
British Pharmacopoeia 2007, and European Pharmacopeia
6 describe the instruction for preparation, uses, and effects
of herbal medicine [7, 100, 101].
Herbal Medicines fortheTreatment ofCOPD
https://t.me/medicina_free
Table 1 Historical evidence of plant herbs found in the ancient scripts
Place/author Book name/year Plants herbs/No. of plant herbs or recipes
Nagpur, Sumerian clay
slab
China, Emperor shen
Nung
India Vedas Turmeric, pepper, Indian sandalwood, clove, nutmeg etc. [93]
Germany, Georg Ebers Ebers Papyrus, 1550 BC 700 plant herbs, such as pomegranate, castor oil plant, onion, g, willow,
Homer’s The Iliad and the odysseys, 800 BC 63 plant herbs, such as Inula helenium L.Asteraceae, and Artemisia etc.
Herodotus 500 BC Plant herbs such as castor oil plant, Orpheus to the fragrant hellebore and
Hippocrates 459-370 BC 300 plant herbs, Wormwood and Centaurium umbellatum Gilib were
Theophrast 371–287 BC, De Causis Plantarium,
John Mesue De re medica, 25 BC-50 AD 250 plant herbs, such as aloe, henbane, ax, poppy, pepper, cinnamon,
Rome, dioscorides De Materia Medica, 77 AD 657 plants herbs, such as fragrant and false hellebore, jimson weed,
Pliny, the elder Historia naturalis, 23 AD 1000 plant herbs, including the Dioscorides work [7]
Avicenna Canon Medicinae, 980–1037 1000 plant herbs [97]
Ibn Baitar Liber magnae collectionis
5000-year-old 12 recipes prepared from 250 plants and herbs [92]
Pen T’Sao, 2500 BC 365 plant herbs, such as Rheirhisoma, camphor, Theae folium,
Podophyllum, ginseng, and ephedra etc. [7]
aloe, garlic, coriander, juniper, etc. [94]
[7]
garlic, and Pythagoras to the sea onion, mustard, and cabbage etc. [95]
applied against fever; opium, henbane, fragrant hellebore, and haselwort
as emetics; garlic against intestine parasites; sea onion, celery, parsley,
asparagus, and garlic as diuretics; oak and pomegranate as astringents;
deadly nightshade, and mandrake were used as narcotics etc. [7]
500 plant herbs such as cinnamon, iris rhizome, false and fragrant
Historia Plantarium
simplicum alimentorum Et
medicamentorum
hellebore, mint, pomegranate, cardamom, and monkshood [96]
the star gentian, cardamom, false hellebore, etc. [97]
henbane, deadly nightshade, poppy, buttercup, willow, camomile, garlic,
nettle, sage, common centaury, coriander, parsley, onion, marsh
mallowivy, sea onion etc. [98]
1000 plant herbs [97]
173
5 Herbal Medicines: AsAordable
Precision Medicine
Despite the development and large production of chemically
synthesized medicine, herbal medicine is mostly used in
developing countries for primary care due to affordability,
safety factor, and local people’s knowledge about herbs.
Now the interest shown by people from developed nations in
using herbal medicine is due to the promotion of health consciousness, prominent effects in treating chronic diseases,
negligible side effects compared to synthetic medicine, and
preparation of the personalized herbal formulation for each
patient. Recently, personalized medicine is replaced by the
term precision medicine, which utilizes the patient's medical
history related to genomics, metabolomics, proteomics, and
environmental factors for preventing, detecting, monitoring,
and curing diseases [102]. By using the omics applications
tools and technologies that are focused on improving the
efcacy of the herbal medicine for the new treatment option
or improving the current treatment, which does not have an
adequate therapeutic effect. The concept of precision medicine can be successful when the accumulation of knowledge
about the methodology to analyze the parameter by advanced
technology, patient clinical and demographical history, and
digital medical electronic equipment’s analysis data can be
gathered for the precise diagnosis of the disease. Precision
medicine for herbal medicine is an unexplored area and
needs a more systematic research and development approach
to validate the data and lead herbal medicine toward increased
therapeutic efcacy [103].
Due to the recent COVID-19 pandemic, the common people are understanding the importance of herbal medicine and
trying to utilize routine herbal medicine and other herbal
supplements to reduce the chance of getting any disease. It
motivated the researchers to explore the eld of herbal medicine and take steps/initiatives toward standardizing precision
medicine for herbal formulation. The diseases which use or
move towards precision herbal medicine mainly include cancer therapeutics, diabetes, hypertension, and HIV/AIDS
[103]. Although precision medicine is developed for COPD
in the case of conventional medicine and herbal medicine is
available for the treatment of COPD, not much attention has
been paid to the development of precision medicine for the
herbal formulation [104–106].
174
https://t.me/medicina_free
S. R. Panda et al.
6 Novel andMarketed Herbal Medicine
Available fortheTreatment ofCOPD
COPD is one of the major concerns for the pharmaceutical
industries; from olden times, there has been extensive use of
novel and herbal mixtures preparations to extravagance
COPD, predominantly in countries of Asia, i.e., China and
India [107]. Herbal medicine and formulations are plantbased or preparation that practices several plant ingredients
in the treatments and curations of preventive and therapeutic
measures [83]. Herbal formulations comprise numerous
dynamic plant-based secondary metabolites containingvarious health assistances against diverse disease symptoms
[108]. Herbal cough syrup, formulated by extracts from
Hedera helix and Thymus vulgaris, is one the most signicant drugs on acceptance in several European countries
[109]. Studies on herbal products containing P. ginseng, H.
helix, S. miltiorrhiza, and some traditional Chinese herbal
medicine decoctions generated encouraging results.
However, interpretation and extrapolation of these results are
difcult for a number of reasons [109, 110].
Oral injection of curcumin is also reported for pointedly
reducing COPD in rats’ cell by reducing the levels of IL-6,
IL-8, and TNF-α after treatment. This shows that curcumin
has potential value in treating and preventing COPD [111].
Echinacea purpurea conventionally been used to avert upper
respiratory contagions [112]. One of the most studied herbal
formulations for the treatment of COPD is Bufeiyishen formula I, II, and III.The main ingredients in the formulation of
different medicinal plants include Panax ginseng, Astragalus
tibetanus, Cornus ofcinalis, Lyciumbarbarum, Schisandra
arisanensis, Fritillaria thunbergia, Perilla frutescens, Citrus
sinensis, Epimedium acuminatum, Paeonia anomala,
Pheretima aspergillum, and Ardisia japonica. Additionally,
secondary metabolites were isolated from them, i.e.,
Ginsenoside, astragaloside IV, icariin, and nobiletin paeonol.
All the authors conducted studies in rats, and they concluded
that Bufeiyishen formula I, reducing airway mucus hypersecretion in COPD [113], also Bufeiyishen formula II, signicantly inhibited mucus hypersecretion, which may be related
to the regulation of the EGFR/PI3K/mTOR pathway [114].
Bufeiyishen formula I exerted its anti-COPD efcacy by
restoring the Th17/Treg balance via activating A2aR, which
may help to elucidate the underlying immunomodulatory
mechanism of BYF and provide evidence for its clinical
application in COPD treatment [115]. Details on different
herbal formulations are given in Table2.
In the market, numerous herbal tablets are also available
as a precaution for COPD.Most of them have positive effects
on lung cleansing, e.g., lung detox tablets from Trurbasics,
Foresta organics, Pure nutrition (Naturals), Nature sure, Gaia
herbs, and Redd remedies. These all-herbal tablets majorly
contain Glycyrrhiza glabra, Echinacea urpurea and
Gingever. The positive effect of G. glabra, and E. urpureaon
COPD were previously reported by many workers [112,
120]. We found herbal tablets from the company Shaleen
name Breath-easy which was particularly reported for
COPD; its herbal formulation has 16 herbs or medicinal
plants, i.e., Salanumsurrsttense, Adhatodavasica,
Glycyrrhiza glabra, Ocimum sanctum, Clerodendrum serratum, Aconitum ferox, Tinospora cordifolia, Zinziber ofcinale, Piper nigrum, Piper longum, Datura mete, Bambusa
arundinacea, Myristica gragrans, Elettaria cardamomum,
Syzygium aromaticum, and Cinnamomum zeylanicum. A list
of commonly used herbal tablets and their compositions is
given in Table3.
Herbal Medicines fortheTreatment ofCOPD
https://t.me/medicina_free
175
(continued)
[113]
[115]
hypersecretion in COPD
the Th17/Treg balance via activating A2aR, which may
help to elucidate the underlying immunomodulatory
Rats Formulation exerted its anti-COPD efcacy by restoring
[116]
mechanism of BYF and provide evidence for its clinical
application in COPD treatment
hypersecretion, which may be related to the regulation of
the EGFR/PI3K/mTOR pathway
[117]
COPD by direct effects on inammatory factor
[118]
decreased levels of serum cytokines such as IL-4, IL-8,
and TNF-α
[118]
Bufei granule can treat patients with stable COPD by
lowering the frequency of acute exacerbation, improving
the quality of life, and alleviating the severity of
[116]
inammation
Expression of numerous interleukins, i.e., IL1𝛽, IL6,
IL8, and IL10 was decreased in peripheral blood and
Rats
[119]
bronchoalveolar lavage uid by formulations treatment
neutrophils in induced sputum; increased expression of
matrix metalloproteinase-9 (MMP-9)
[120]
by restraining inammation of the patient
Boiling Rats Formulation was reported for reducing airway mucus
S.No Herbal formulations Method Type of study Results References
1 Bufeiyishen formula III
Table 2 List of herbal formulations studied in COPD patients or in animal models
Decoction and steam
sterilization
Composition: Ginsenoside, astragaloside IV,
icariin, nobiletin paeonol and N-acetylcysteine
Ingredients: 9 g Panax ginseng rhizome, 15 g
Astragalus tibetanus rhizome, 12 g Cornus
2 Bufeiyishen formula I
ofcinalis fructus, 12 g Lyciumbarbarum fructus, 9
g Schisandra arisanensis fructus, 9 g Fritillaria
thunbergia bulbus, 9 g Perilla frutescens fructus, 9
g of Citrus sinensis Pericarpium, 9 g of Epimedium
acuminatum folium, 9 g Paeonia anomala rhizome,
12 g Pheretima aspergillum herba, and 15 g Ardisia
japonica herba
Boiling Rats Formulation signicantly inhibited mucus
3 Bufei yishen formula II
Decoction Humans Formulation was reported to have positive inuence on
Composition: Ginsenoside, astragaloside, icariin,
paeonol, nobiletin
Ingredients: Ephedra, almonds, gypsum, and
licorice. The specic ratio of ephedra and gypsum
4 Maxing shigan
Decoction Humans Increased FEV1, FVC, and peak expiratory ow;
is 1:2
Ingredients: Ephedrae sinicae herba, Cinnamomi
5 Xiaoqinglong
ramulus, Pinelliae rhizome, Zingiberis rhizome,
Asari Radix rhizome, Schisandrae Chinensis
fructus, Paeoniae Alba radix, Glycyrrhiizae radix
Boiling with water Humans
Ingredients: 8 g/bag of Codonopsis rhizome,
Rehmanniae Praeparata rhizome, Corni fructus,
6 Bufelikeli
Decoction and steam
Ephedra Sinicaherba, and Pericarpiumcitri
reticulatae
7 Bufeiyishen
sterilization
Ingredients: 15 g Astragalus tibetanus rhizome, 15
Decoction Humans Decreased the total cell counts and percentage of
g Panax ginseng rhizome, 15 g Corni fructus, and 9
g Schisandrae arisanensis Fructus
8 Xiaoqinglong
Ingredients: Ephedraesinicae, Cinnamomiramulus,
Pinelliae rhizome, Zingiberis rhizome, Asari
rhizome, Schisandrae chinensis Fructus, Paeoniae
Decoction Humans Formulation plays an important role in COPD treatments
alba radix, Glycyrrhiizae radix
Ingredients: Ophiopogonis rhizome, Ginseng
rhizome, Glycyrrhizae rhizome, Pinelliae rhizome,
Phragmitis rhizome, Coicis semen, Benincasa
hispida, Persicae semen
9 Qianjinweijing
176
https://t.me/medicina_free
S. R. Panda et al.
[121]
TNF-α; increased the level of IFN-; lowered the ratio of
IFN- and IL-4 (Th1/Th2) compared to control rats in the
[122]
homogenate of lung tissue from rats with COPD and
syndrome of phlegm-heat obstructing lung
on COPD patients, can relieve cough, phlegm and
[123]
asthma symptoms, improve lung function, and conform
to the treatment principles of COPD
COPD in man
Humans Formulation did not appear to substantially affect the
Decoction Rats Decreased levels of cytokines such as IL-4, IL-8, and
Ingredients: Ephedrae sinicae,
Armeniacaeamarum, and glycyrrhizae
S.No Herbal formulations Method Type of study Results References
10 Maxing Shigan
Table 2 (continued)
Decoction Humans Clinical study conrm that formulation has a good effect
11 Bushennaqihuoxue
Ingredients: Ginseng, clams, fairy spleen, walnut
meat, psoralen, schisandra, danshen, safower,
Boiling of plant
extract in water
peach and kernel
Ingredients: 10 g Ophiopogonis tuber, 5 g Oryza
sativa, 5 g Pinellia ternate, 3 g Ziziphus jujuba, 2 g
12 Bakumondo
Panax ginseng and 2 g Glycyrrhiza root
Соседние файлы в папке Библиотека им академика М.И. Перельмана