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Role ofNatural Polysaccharides
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intheManagement ofLifestyle
Diseases
ShuvamSar, TanmoyBanerjee, AnkitKumar, ArunBaidya,
SaptapadiSaha, JayashreeMondal, RituparnaChaki,
AmitKumarHalder, andNilanjanGhosh
Abstract
Metabolic syndrome (MetS) affects 20–25% of adults and
as many as 19.5–20% of adolescents. MetS negatively
impacts multiple physiological processes. Natural compounds have an exceptionally bright aspect with a promising alternative to synthetic medications. Plant
polysaccharides (PPSs), which are made up of at least ten
monosaccharides, exhibit excellent safety and a range of
pharmacological actions, such as anti-apoptotic, antihyperglycemic, antihyperlipidemic, antioxidant, and antibrotic benets. However, the benets of numerous PPS
for metabolic disorders, including gastroesophageal
reux disease, cardiovascular disease, chronic renal disease, and pulmonary diseases, are often brought on by a
malfunction in the metabolism of lipids, glucose, and
peptides. Therefore, the quantity of articles focusing on
antioxidative PPSs have steadily increased over the past
decade. This chapter outlines numerous attributes and cellular mechanisms of several PPS in metabolic disorders.
In addition, the interaction of PPS with various genes and
proteins involved in molecular signaling pathways is
briey elucidated.
Keywords
Metabolic disease · Plant polysaccharides · Inammatory
mediators · Molecular signaling · mRNA expressions
S. Sar · T. Banerjee · A. Kumar · A. Baidya · S. Saha · J. Mondal ·
N. Ghosh (*)
Department of Pharmaceutical Technology, Jadavpur University,
Kolkata, West Bengal, India
e-mail: nilanjanghosh.phamacy@jadavpuruniversity.in
R. Chaki · A. K. Halder
Dr. B.C.Roy College of Pharmacy and Allied Health Sciences,
Durgapur, India
1 Introduction
Lifestyle diseases occur due to the unhealthy habits of people which detract them from the regular activities and lead
them to a sedentary routine causing various health problems
that can be even to some extent lethal. In a broader sense,
non-communicable or non-infectious diseases are generally
caused due to malfunctioning of metabolism regulator
enzymes, eventual accumulation of primary and secondary
products of metabolism, and deciency of desired molecules
for biochemical reactions. These diseases are known as metabolic disorders/diseases (MDs) or non-communicable diseases (NCDs). So, it can be said that all non-communicable
diseases in a sense are metabolic disorders. This chapter
focuses on metabolic disorders arising from lifestyle changes
in modern days. There might be various forms of metabolic
diseases, but the primary causing factor lies between the
junction of hyperglycemia and hyperlipidemia. Disturbances
in the homeostasis of blood glucose level and free fatty acid
(FFAs) level rise as the initiation point of all cardiovascular,
hepatic, and nephrological diseases. Diabetes works longer
and in a deeper way than hyperlipidemia. Prolonged insulinemia and hyperglycemia gradually accumulate fat globules in adipose tissues of liver, gastrointestinal viscera, and
other parts of body. Concomitantly prolonged deposition of
lipid in the abdominal area becomes the factory of glucose
through neoglucogenesis and other pathways. Chronic kidney/renal disease usually occurs as a consequence of diabetic
toxicity leading to death. Similarly, cardiovascular and
hepatic metabolic ailment may serve lethal for patients. MDs
kill about 40 million people each year, which is nearly 70%
of all death around the globe. Thus, meeting this crisis
through correct treatment approach is of current interest to
researchers [1].
The formation and progression of MDs, such as diabetes,
obesity, cardiovascular diseases (CVDs), and non-alcoholic
steatohepatitis, are caused by biomolecules such as glucose,
protein, fat, vitamins, and minerals in the body that are not
metabolized effectively. These MDs are the result of a com-
© 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_21
415
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plicated interaction between diet, susceptibility, genetics,
and epigenetics. MDs are caused, to a massive extent, by
social and behavioral risk factors, like smoking, unhealthy
diet, less physical activity, reckless alcoholism, and unsurpassable stress in work–life balance. Obesity or rising blood
lipids, elevated blood glucose, and raised high pressure are
the root causes of numerous deadly problems in the cardiovascular, respiratory, and renal systems. Many of the risk
factors are common for a number of MDs. According to the
WHO, smoking causes the deaths of more than seven million
people each year, and that gure is expected to rise. Excessive
consumption of dietary sodium kills 4.1 million people annually, while alcohol consumption leads to approximately 1.65
million deaths from NCDs. Simple lack of exercise kills 1.6
million people a year [2].
2 General Pathophysiology
ofMetabolic Diseases
MDs have a continuously progressive pathophysiological
state comprising several interdependent phenomena like
inammation, ectopic (especially liver and muscle) and visceral obesity, insulin resistance. The inammatory and prethrombotic markers, C-reactive protein (CRP), synthesized
and secreted by hepatocytes, insulin levels, plasminogen
activator inhibitors, leptin, adiponectin, resistin, tumor
necrosis factor-α (TNF-α), leptin, monocyte chemoattractant
protein-1 (MCP-1), interleukin-6 (IL-6), uric acid (UA) levels, and microalbuminuria are considered to better understand the molecular scenario of MDs [3]. Obesity, abdominal
adiposity, hypertension, and hyperglycemia are common
signs of various metabolic diseases. IkB kinase and c-Jun
terminal kinase (JNK), two pro-inammatory serine kinases
that are activated by FFA buildup, help to release IL-6 from
adipose tissue. Additionally, elevated FFA encourages
hepatic protein kinase activation, which results in gluconeogenesis and lipogenesis. These lead to components of MDs
such as IR, lipotoxicity, altered glucose metabolism, and atherosclerosis [4]. The evolution of CVDs such as atherosclerosis, hypertension, heart failure, and peripheral artery
disease can be sped up by IR because it promotes the generation of reactive oxygen species (ROS) and causes an imbalance in the enzyme endothelial nitric oxide synthase (eNOS)
[5].
3 Plant Polysaccharides andIts
Composition
The most prevalent naturally occurring macromolecular
polymer may be found in polysaccharides, which are produced by bacteria, fungus, plants, and even algae [6]. A variety of monosaccharides are combined to form polysaccharide
structures, which are joined together by glycosidic linkages.
Numerous research suggest that plant polysaccharides
(PPSs) exhibit a variety of biological activities including
immunomodulation, antineoplasia, anti-inammation, antiviral, antioxidative, osteogenesis, hypolipidemic and hypoglycemic effects. Despite PPSs’ potency, there are still
signicant drawbacks, including poor targeting, unstable,
quick blood clearance rate, and unfocused scope of action,
which substantially impair bioavailability and clinical use.
Recent studies have found that PPSs molecular weights
can be up to thousands or even millions. Hydrophilic groups
such as OH, COOH, and NH2 groups can form bioadhesive
layers with epithelial and mucosal tissues [7]. The most common component of polysaccharides is d-glucose. However,
d-fructose, d-galactose, l-galactose, d-mannose, l-arabinose,
rhamnose, fucose, uronic acid, and d-xylose also can be
found as depicted in Fig.1 [8]. Amino sugars are one type of
monosaccharide derivative found in polysaccharides. Some
plants contain their derivatives (N-acetylneuraminic acid and
N-acetylmuramic acid) as well as the monosaccharide acids
(glucuronic acid and iduronic acid) [9].
OH
OH
HO
HO
Fucose
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417
HO
D-Glucose
D-Mannose
OHO
OH
O
OH
OH
OH
OH
HO
D-Fructose
O
HO
OH
L-Arabinose
OHHO
OH
OH
HO
O
OH
OH
HO
OH
OH
OHO
D-Galactose
O
OH
OH
OH
D-Xylose
OH
O
OHOHOH
L-Galactose
OH
OH
OH
Rhamnose
OH
O
OH
OHO
HO
OH
OH
Fig. 1 Structures of components of polysaccharides
4 Management ofLifestyle Disorders
Using Natural Polysaccharides
4.1 Hyperglycemia
Hyperglycemia is the name of the condition or symptom
caused by diabetes mellitus, which is characterized by insufcient insulin secretion, IR, or reduced sensitivity of the target organs to insulin when it is secreted normally, followed
by consequences of MDs. β cells of the pancreas secrete
insulin, but due to the lack of sensitivity of target organ cells,
insulin cannot bind to the corresponding receptors upon the
cells, and as a result, the secreted insulin stays in the blood
for long, causing hyperinsulinemia. However, when the body
cannot maintain normal blood sugar level through the feedback mechanism in insulin-glucagon concentration, they
develop type 2 diabetes mellitus (T2DM). Hyperglycemia is
the main among MDs that in turn gives rise to several other
organ system disorders, like chronic renal failure (CRF), cardiac diseases, hyperlipidemia, nervous system diseases, etc.
That is why hyperglycemia is known as the silent killer. One
of the main stimulators of T2DM is obesity alone, particularly abdominal adiposity. Consumption of high-fatcontaining foods, fast foods made with highly saturated oils,
lack of exercise, and an overall sedentary lifestyle are the
underlying causes of abdominal accumulation of fats. In case
of abdominal fat, lipid is deposited within adipocyte cells of
adipose tissue, in the abdominal area which works as source
of calorie supply in fasting [10]. But when adipocyte cells
accumulate lipids more than their normal capacity, due to
high-fat diet intake and sedentary lifestyle, they lead to
hepatic and systemic insulin resistance through interlukin-6
(IL-6) and other adipose-specic cytokines [11]. This is very
clear that no other metabolic diseases are so directly linked
to lifestyle than hyperglycemia. Not only fatty foods, fast
food consumption, and irregularity in having breakfast,
lunch, and dinner also lead to the development of hyperglycemia. That is why modern views portray hyperglycemia and
hyperlipidemia as linked to each other, as their further complications also progress simultaneously (summarized in
Fig.2).
Polysaccharides acting against hyperglycemia with their
sources and probable mechanisms of action are hereby summarized in Table1.
4.2 Hyperlipidemia
Hyperlipidemia is the second-most prevalent metabolic disorder that has been occurring from the dawn of modern days,
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Fig. 2 Interlink between hyperglycemia, obesity, hypertension, and CVDs and action of natural polysaccharides on them
mostly due to the high intake of fatty foods and consequently
the gradual rise in FFAs, triglycerides (TGs), cholesterol,
absorption. Thus, lowering the intestinal absorption of cholesterol is another way to avoid hyperlipidemia [29].
and low-density lipoprotein (LDL-C) levels and decreasing
high-density lipoprotein (HDL-C) cholesterol levels. This
4.2.1 Polysaccharides Against Hyperlipidemia
occurs due to unhealthy lifestyles including high-fat diet and
other lifestyle behavioral factors. Evidence indicates that
smoking can disrupt lipid metabolism. Surprisingly, eating
betel nuts increases the risk of hyperlipidemia as well as
increasing the likelihood of obesity because it increases hunger by blocking GABA receptors. Cardiovascular disorders
including atherosclerosis and coronary heart disease are
caused by persistent hyperlipidemia [27]. With the constant
changes in lifestyle, environment, and food habits, more and
more people suffer from this and its consequences. Therefore,
downregulating serum lipid levels is the ultimate way to prevent the risk of hyperlipidemia. Additionally, aberrant adipokine synthesis, including that of adiponectin and leptin, is
linked to hyperlipidemia [28]. Cholesterol, after being
4.2.1.1 Cyclocarya Polysaccharide
The “sweet tea tree” is another name for the species
Cyclocarya paliurus (Batal) Iljinskaja. By slowing fatty acid
production and degrading fatty acids, Cyclocarya paliurus
polysaccharide (CPP) has been found to reduce FFAs in
KKAy mice. In addition, there is evidence that CPP causes
an increase in the expression of adipose triglyceride lipase
(ATGL) and peroxisome proliferator-activated receptor
(PPAR) and a relative decrease in FFAs and hepatic
3-hydroxy-3-methyl glutaryl-Coenzyme-A (HMG-CoA)
mRNA. Downregulating the expression of HMG-CoA
reductase prevents the liver’s production of new cholesterol,
hence lowering blood cholesterol levels [30].
absorbed from the intestine, is transported through the chylomicron to the liver. The cholesterol absorption route is crucial for treating hyperlipidemia because of the intimate
connection between lipid metabolism and cholesterol
4.2.1.2 Pleurotus Mycelia Polysaccharides
The polysaccharides are extracted from mycelia of Pleurotus
eryngii var. tuoliensis, a medicinal mushroom that belongs to
the family Pleurotaceae of the phylum Basidiomycota. It has
Role ofNatural Polysaccharides intheManagement ofLifestyle Diseases
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Table 1 Polysaccharides acting against hyperglycemia
Plant polysaccharide Biological source Research model Action on parameters Remarks References
Codium fragile
sulfated
polysaccharide
(CFSP)
Alhagi
polysaccharide
(neutral Aps-1, acidic
Aps-2 and 3)
Polysaccharides from
Adlay seeds (PAS)
Acanthopanax
polysaccharide
(ASP)
Grifola
polysaccharides
Astragalus
polysaccharide
Cordyceps
polysaccharide
Fructus
polysaccharide
Tea polysaccharide Camellia sinensis L.High-fat diet and
The protein-bound
polysaccharide from
pumpkin fruits
(PBPP)
Codium fragile
alga
Alhagi
pseudalhagi
Coix lacryma jobi
L., commonly
known as adlay
Acanthopanax
senticosus
Grifola frondosa KK-ay mice
Dried roots of
Astragalus
membranaceus
Fruiting bodies of
Cordyceps
sinensis
Fructus corni
Pumpkin fruits Alloxan-induced
Alloxan-induced
diabetic rats
In vitro Antioxidant effects in DPPH
8weeks old ICR
male mice
Alloxan-induced
diabetes mice
Hep G2 cells
Fat-fed
streptozotocintreated T2DM rats
Streptozotocin and
nicotinamide
induced diabetic
male Wistar rats
Streptozotocininduced diabetic rats
RIN-m5f cells (in
vitro)
streptozotocininduced male
Kunming mice
Sprague-Dawley rats
Decrease in blood glucose
and intestinal amylase levels
Enhanced antioxidant
enzymes activity
and ABTS assays
α-Glucosidase inhibition and
ABTS scavenging activity by
APs-3
Decreased blood glucose and
insulin levels
Reduced plasma levels of
amyloid β42 and glycated
hemoglobin (HbA1c)
Increased expression of
glucagon-like peptide-1
(GLP-1) and superoxide
dismutase (SOD) activity
Lowered fasting blood
glucose level and blood
insulin level
Lowered blood glucose and
reversed insulin resistance
Enhanced glucose uptake
Decreased plasma glucose
level
Improved response in OGTT
and lowered post-prandial
blood glucose level
Lowered blood glucose level
and reversed insulin
resistance
Hypoglycemic action Hypoglycemic action
Hypoglycemic action [21]
Increased glucose tolerance
and lowered α-amylase
activity
Improved lipid prole
Hypoglycemic activity
through free radical
scavenging action
Not a very potent
anti-diabetic
Good antioxidant
Signicant hypolipidemic
action
Hypoglycemic action by
α-glucosidase inhibition
and insulin sensitization
Increased
phosphorylated-AktSer473
Synthesis of intracellular
glycogen through the Akt/
GSK-3 pathway
Normalized insulin-induced
PKB-Ser473
phosphorylation and
GLUT-4 translocation in
skeletal muscle
Reduced PTP1B protein
level and activity in the
muscle, but not in the liver
along with NF-kB
activation
α-Amylase and
α-glucosidase inhibition
Increased insulin secretion
and promoted pancreatic
β-cell proliferation
through PI3Kp85/p-Akt/
GLUT4 signaling pathway
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
(continued)
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Table 1 (continued)
Plant polysaccharide Biological source Research model Action on parameters Remarks References
Nigella seed
polysaccharide
Polysaccharides from
Hovenia (Guaizao)
Sargassum
polysaccharides
Suillellus
polysaccharides
AAMP-N Armillaria mellea
Nigella sativa
seed
Hovenia dulcis
Sargassum
fusiforme
Suillellus luridus
fruiting body
High-fat diet and
streptozotocininduced Kunming
mice
Streptozotocininduced diabetic
male SpragueDawley rat
High glucose and
high-fat diets fed
T2DM mice
Streptozotocininduced diabetic
male ICR mice
Db/db mice
Hepa 1–6 cells
Lowered fasting blood
glucose (FBG), glycosylated
serum protein (GSP),
TG, TC, LDL-C,
Malondialdehyde (MDA),
TNF-α, IL-6, and IL-1β
Insulinemia. Raised HDL-C,
total antioxidant capacity
(T-AOC), SOD, catalase
(CAT), and p-AKT and
GLUT4 expression
Lowered FBG.Higher body
weight, and liver glycogen
levels
Insulinemia
Improved insulin resistance.
Fasting blood glucose (FPG)
and fasting insulin (FINS)
were signicantly decreased
Lowered insulin resistance
(IR)
Expression of Glut-2in
pancreatic tissue is increased
Blood glucose level reduced
to normal
Decline in insulin level
Signicantly reduced blood
glucose level
Antagonized insulin
resistance
Hypoglycemic action was
done by PI3Kp85/p-Akt/
GLUT4 pathway
Hypoglycemic mechanisms
may include balancing the
regeneration and apoptosis
of β-cells and activating
liver
glycometabolism-linked
Signaling pathways in
diabetic rats
Increased insulin sensitivity [25]
Phosphorylation of insulin
receptor and AKT
S. Sar et al.
[22]
[23]
[24]
[26]
been proved that zinc-containing polysaccharides show antioxidant properties. Additionally, it has been demonstrated
that natural alkali-extractable (AlMZPS) and acidic
(AcMZPS) compounds both dramatically raise HDL-C levels and lower blood levels of LDL-C, VLDL-C, TC, and TG,
therefore establishing their hyperlipidemic effects [31].
4.2.1.3 Ulvan
Ulvan polysaccharide (PU3) has been isolated from Ulvan
pertusa, a green alga. The administration of PU3 has shown
inhibition of lipid peroxidation in hyperlipidemic mice by
increasing and activating antioxidant enzymes. PU3 lessen
risk factors rising from interrelation between oxidative stress
and hyperlipidemia [32].
4.2.1.4 Morchella Polysaccharides
Morchella esculenta polysaccharides (EnMPS and MPS
fractions) from Morchella mushroom is a large complex carbohydrate. Following administration of both fractions,
higher HDL-C and lower LDL-C values were seen, indicat-
ing a possible inhibition against hyperlipidemia-derived liver
damage. These 2 fractions also have protective action against
oxidative stress-induced hyperlipidemic complications.
EnMPS has been found to enhance the antioxidant enzyme
activities and reduced the myeloperoxidase (MPO) content,
both invivo and invitro experiments [33].
4.2.1.5 TDGP-3 Polysaccharides
Traditional Chinese medicine uses a kind of Vitaceae plant
called Tetrastigma hemsleyanum Diels et Gilg (TDGP3). A
lipid metabolic pathway that is out of balance might result
from too many free radicals and the subsequent oxidative
stress, which can result in hyperlipidemia. In vivo, TDGP-3
has demonstrated strong antioxidant activity, lowering LDLC, TC, and TG levels while raising HDL-C levels [34].
4.2.1.6 Pine Needle Polysaccharide (PNP)
Pine needle polysaccharide (PNP), extracted from the Pinus
massoniana tree has shown hypolipidemic and antioxidant
effects. High-fat diets can increase the production of free
Role ofNatural Polysaccharides intheManagement ofLifestyle Diseases
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421
radicals and weaken the antioxidant defense system. Because
oxidized-LDL-C, which is intimately linked to the development of hyperlipidemia, is produced when reactive oxygen
species (ROS) oxidize LDL-C.PNP increases antioxidant
enzymes and non-enzymatic antioxidants, reducing oxidative damage in mice subjected to HFD [35].
4.2.1.7 Selenium Modied Lachnum Polysaccharide
Lachnum is a saprophytic fungus with various biological
actions. SeLEP-1b, an organically modied selenium containing Lachnum polysaccharide, effectively reduced lipids
and protected the liver. SeLEP-1b had shown hypolipidemic
action probably by reducing the expression of the genes for
fatty acid synthase (FAS) and adipocyte fatty acid binding
protein (aP2), which are involved in TG production and lipid
storage in adipocytes. Another possibility is that SeLEP-1b,
which downregulates the liver x receptor ligands known as
the major regulators of lipid metabolism, increased lipid
metabolism and broke down the fat and cholesterol in the
liver. The HMG-CoA reductase enzyme in the liver may be
inhibited to reduce cholesterol production, which would be
the third possible cause [36].
4.2.1.8 Prunella Polysaccharides
The Prunella vulgaris L. (Labiatae family) plant is the source
of the Prunella vulgaris polysaccharides, which are also
referred to as “self-heal” in Western herbal therapy. PVPs
markedly decrease plasma TC, TGs, and LDL-C levels and
increased HDL-C in high-fat/high-cholesterol (HFHC) dietfed mice. PVPs also lowered MDA and TNF-α levels in
hyperlipidemic rats and stimulated glutathione peroxidase
(GSH-Px), indicating its antioxidant property [37].
4.2.1.9 Apostichopus Polysaccharides
Apostichopus japonicus polysaccharide (AJP) is obtained
from sea cucumber Apostichopus japonicus Selenka (also
identied as Stichopus japonicus Selenka). HDL-C levels
were raised, while TC, TG, and LDL-C levels signicantly
decreased, following AJP administration, which proves the
biosynthesis and uptake of cholesterol. To modulate cholesterol metabolism, AJP interacts with lipids and functions as
a carrier, improving the transit and excretion of serum lipids.
AJP can also act as bile acid synthesis stimulators. Synthesis
of bile acids depletes hepatic cholesterol [38].
4.2.1.11 Helvella Polysaccharides
The treatment of high doses of Helvella polysaccharides
(HLP), obtained from Helvella leucopus, also named Bachu
mushroom, partially delayed the uprising serum LDL-C
level, and HDL-C decrease. The effect was comparable to
atorvastatin treatment, correlated with the reduction in serum
TGs [40].
4.2.1.12 Ganoderma Polysaccharides
The primary active ingredients of Ganoderma lucidum (GL),
a Chinese herbal remedy that has been used for millennia in
Asia, are Ganoderma lucidum polysaccharides (GLP),
which, depending on the dose, show immunoregulatory,
antioxidant, and hypolipidemic effects [41].
4.2.1.13 Quinoa Polysaccharide
The Incas is formerly referred to the Andean pseudo-cereal
quinoa (Chenopodium quinoa Willd., family Amaranthaceae)
as the “mother of all grains.” Quinoa seed eating has been
linked to reduce blood TG and LDL-C levels invivo [42].
4.2.1.14 Holothuria Polysaccharides
Holothuria leucospilota polysaccharides (HLP), obtained
from dry black sea cucumbers. Alleviated high-fat diet
induced hyperlipidemia. HLP is difcult to digest in the
upper gastrointestinal tract, so in the large intestine it is converted to short-chain fatty acids (SCFAs) by gut microbiota
and regulates lipid metabolism. HLP has been reported to
suppress acetyl-CoA carboxylase (ACC) and fatty acid
translocase CD36 expressions to inhibit lipid accumulation
in liver cells, thereby secretion of excess leptin and adiponectin from adipocytes was inhibited. Leptin and adiponectin stimulate inammatory factors and insulin secretion is
elevated, leading to IR.HLP also downregulated the expressions of TNF-α and NF-kB, which directly alleviated hyperlipidemia [43].
4.2.1.15 Rice Bran Polysaccharide
Rice bran polysaccharide (RBP) is got from the rice (Oryza
sativa L.) milling. RBP-mediated modulation of expressions
of PPARs, ACC, FAS, sterol regulatory element-binding protein 1 (SREBP-1C), sirtuin 1(SIRT1) in HFD-induced mouse
model implies that RBP might be candidate for adjuvant
therapies for hyperlipidemia [44].
4.2.1.10 Termitomyces Polysaccharides
Two fractions, EIPS and AIPS are hydrolysis products of
intracellular polysaccharide from the fruiting bodies of
Termitomyces albuminosus, also known as “Chicken
Mushroom” or “Jizong” in China. Treatment EIPS lowered
the serum lipids and restored lipid metabolic disturbances
induced by high-fat emulsion [39].
4.2.1.16 Pleurotus Polysaccharides
In a zebrash hyperlipidemia model, it has been demonstrated that polysaccharides from the fruiting bodies (PEPE)
of Pleurotus eryngii (king oyster mushroom) may reduce the
lipid level during the lipid absorption phase. Although it has
considerable toxicity, it can signicantly reduce the amount
of oxidized LDL-induced foam-cell production in murine
macrophage cells (RAW264.7) [45].
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S. Sar et al.
4.3 Hypertension
Long-term hypertension results in ultimate organ failure and
is dened as an increase in blood pressure (BP) that is more
than systolic 130–139/diastolic 85–89 mmHg. Arterial
hypertension is a major risk factor because of its consequences like coronary heart disease, left ventricular hypertrophy, and renal diseases. The involvement of target organs
(i.e., heart, brain, and kidneys) implies the severity and fatality of the outcome. In addition to mediating vasodilation, the
endothelium releases nitric oxide (NO), which controls leukocyte adherence to endothelial cells and lowers the production of peptides that constrict blood vessels and raise blood
pressure. Hypertension results from reactive oxidative stress
signaling, which also causes vascular inammation and persistently elevated vascular tone [46].
Hyperglycemia and hyperlipidemia directly or indirectly
cause hypertension. Although most of the causal factors lie
in lifestyle habits. A sedentary lifestyle, lack of physical
exercise, consumption of food with high salt, sugar, and oil
content, smoking, alcoholism, regular stress at work and
social life, and lack of deep enough sleep widen the scope for
hypertension to occur [47].
4.3.1 Polysaccharides Used Against
Hypertension
4.3.1.1 Cordyceps Polysaccharides
Caterpillars are parasitized by a fungus called Cordyceps
sinensis. Systolic and diastolic blood pressure (SBP and
DBP) were demonstrated to be susceptible to reduction by C.
sinensis polysaccharides (CSP1) in spontaneously hyperten-
sive rats. Additionally, it increased NO, lowered the levels of
epinephrine, noradrenaline, endothelin-1 (ET-1), and
angiotensin II (Ang-II), and repressed the release of TGF-I
and CRP [48].
4.3.1.2 Watermelon Rinds Polysaccharide
Watermelon polysaccharides (WMRP) are extracted from
Citrullus lanatus rinds by hot water. WMRP exhibited ACEinhibitory action in a dose-dependent fashion probably by
the galacturonic acid present in the extract. The acidic pH
might have denatured the ACE enzyme also [49].
4.3.1.3 White Mulberry Fruit Polysaccharides
In Sprague-Dawley rats, white mulberry fruit polysaccharides (WMFPs) from the mulberry (Morus alba) of the family Moraceae have been demonstrated to boost NO production
and relax blood vessels. After receiving WMFP treatment,
rats’ mean artery pressure (MAP) decreased by more than
10%, establishing a NO dependent pathway [50].
4.3.1.4 Althea Polysaccharides
Water-soluble acidic bioactive polysaccharides are present in
the whole plant Althea rosea is also known as “saze posh.”
The dose-dependent ACE-inhibitory effect of Althea polysaccharides has been seen in studies. Plant mucilages can
reduce blood pressure by lowering endothelial dysfunction
and decreasing inammation in the vasculature, through the
blockage of HMGCoA formation [51].
4.3.1.5 Sodium Alginate Oligosaccharides
A ber-rich polysaccharide called alginate is obtained from
seaweeds like kombu and giant kelp. Dahl S rats treated with
sodium alginate oligosaccharide demonstrated a dosedependent attenuation against salt-induced hypertension.
The BP signicantly declined after alginate administration
and was maintained throughout the experiment [52].
4.3.1.6 Undaria Polysaccharide
An Undaria pinnatida (Qundaicai) brown alga fucoidan-
rich sulfated polysaccharide showed signicant antihypertensive effects on vascular relaxation both invivo and
invitro. Along with reducing blood pressure in chronically
hypertensive rats receiving L-NAME treatment, this medication also protects the thoracic aorta’s histological structure
through activating the Akt/eNOS pathway. Fucoidan reduced
the elevated inducible nitric oxide synthase production and
systemic inammation in those animals [53].
4.3.1.7 Other Polysaccharides
Polysaccharide from Xin-Ji-Er-Kang (XJEK), the Chinese
medicine, exerts protection against L-NAME-induced hypertensive mice and Ang II-induced damage in human umbilical
vein endothelial cells (HUVECs) and it might be done by
improving endothelial function and the inammation in
blood vessels [54]. Cystoseira crinita sulfated polysaccharide shows anti-hypertensive action through ACE inhibition
[55]. By triggering the eNOS/NO signaling pathway, astragalus polysaccharides decreased the MPA pressure in rats
with monocrotaline-induced pulmonary arterial hypertension [56]. Acidic polysaccharides from Gastrodia rhizome,
Chickpea water-soluble polysaccharide, Cymodocea nodosa
sulfated polysaccharide, Momordica charantia polysaccha-
ride, polysaccharides from Ephedra alata, Almond and
Pistachio not only alleviate vasoconstriction by downregulating angiotensin II, but also decreased vasodilator bradykinin metabolism by blocking kininase II [57]. Polysaccharide
as the active constituent of Dendrobium ofcinale can reverse
metabolic hypertension in rats by activating the intestinal
SCFAs-GPCR43/41 pathway [58]. Acidic polysaccharides
from Gastrodia elata Blume rhizome have shown a reduc-
tion in hypertension and improved serum lipid levels [59].
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