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extract 125 mg, ashwagandha extract 300 mg or identical placebo twice daily for
eight weeks as a capsule. A signicant improvement in the PSS scale was observed
in 58 volunteers (who completed the trial) with a marked drop in blood cortisol levels as well as improved sleep pattern. Another clinical study focused on treating an
obese adult population with 300 mg of ashwagandha root extract (>5% withanolides)
twice a day for 10 weeks. This has led to decreased levels of cortisol in the blood,
body weight and basic metabolic index, as well as decreased body fat. A preclinical
study in rats showed decreased corticosterone levels in the hippocampus in the stress
model (Baitharu et al, 2013). The other mechanism by which WS alleviates stress
is by immune stimulation and anti-inammatory effects. This leads to an increase
in the number of peripheral T cells (CD3, CD4 and CD8 populations), interleukin-2
(IL-2), interferon gamma (INF-γ) and the number of polymorphonuclear leukocytes,
which are downregulated in stress. Preclinical studies using WS extracts and withanolides-rich extracts (2.7%) on stress induced in rats by cold restraint stress and
forced swimming-induced stress, showed antistress activity with increased white
blood cell counts, neutrophils, lymphocytes and eosinophils (Anju, 2011; Puri and
Puroh it, 2016). Panax ginseng, another antistress plant of the family Araliaceae,
contains active phytoconstituents that reduce stress including ginsenoside Rb1 and
Rg3. Stress results in decreased brain brain-derived neurotrophic factor (BDNF) levels altering heat shock protein – 70 in the hippocampus. BDNF is synthesised in the
endoplasmic reticulum and plays its functions by binding on the tropomyosin receptor kinase B receptor further activating the signal transduction cascade to promote
neuroplasticity, neuronal survival and differentiation (Lee and Kim, 2010).
Clinical study of Korean red ginseng (KRG) in two high-stress occupations, that
is, nurses and reghters aged 20–60 years were included in the study (Baek et al,
2019). The stress levels of these volunteers and cognition were assessed using the
Beck Depression Inventory and the Stress Response Inventory. Chronic stress in
volunteers had raised levels of cortisol and catecholamine, adrenaline and reduced
triglycerides. Treatment with KRG for 2 g/day of KRG (LAX-101) or placebo for
6weeks showed reduced levels of cortisol and epinephrine and normalised triglycerides. This is assumed to be the possible mechanism for central nervous system (CNS)
stabilisation. Further, KRG was found to contain Rb1, 6.44 mg/g; Rb2, 2.25 mg/g;
Rc, 2.68 mg/g; Rd, 0.50 mg/g; Re, 2.08 mg/g; Rf, 0.89 mg/g; Rg1, 3.21 mg/g; Rg2,
0.29 mg/g; Rg3, 0.18 mg/g. Treatment with Rb1 also increases the levels of thermal shock protein 70 and BDNF that have neuroprotective and anti-stress properties
(Kim et al, 2013). A pre-clinical study consisting of total ginseng panax saponins
(TSPG) was studied on chronic unpredictable mild stress (CUMS)-induced stress in
rats. They were treated with TSPG (50 mg/kg/day, 100 mg/kg/day) during the entire
modelling period. TSPG was found to improve depressive behaviour and to exhibit
neuroprotection. TSPG inhibited pro-inammatory cytokines, as well as P38 and
Jun N-terminal kinase (JNK) protein phosphorylation in the hippocampus, indicating signicant antidepressant and antistress activity. Camellia sinensis L. commonly
called green tea from the Theaceae family. The active phytoconstituent, L-theanine
is thenon-proteinogenic amino acid, passes freely through the blood-brain barrier,
acts by reduction of presynaptic glutamate release, increased inhibitory neurotransmitter GABA, and enhanced glycine and dopamine release (Kakuda et al, 2008;
NeuroPhytomedicine
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Shen et al, 2019; Yamada et al, 2007). Clinical study on fth-year college students
(n = 20) of the school of pharmaceutical sciences, practising outside the university
at the hospital or a drug store, for 11 weeks, where they were administered theanine
(200 mg, twice a day, after breakfast and lunch). These were assessed for anxiety
using a state anxiety inventory test. At the end of the study, treatment with théanine
supplementation was found to be benecial in suppressing psychosocial stress. It was
assumed that theanine improved the HPA axis (Unno et al, 2013).
87
5.3 PHYTOCONSTITUENTS USED FOR ANXIETY
People who experience anxiety have difculty with their sleep habits, their ability to
focus and their ability to interact with others. Anxiety disorders like panic disorder
are characterised by recurrent, unprovoked panic attacks that leave sufferers feeling
extremely anxious, approaching doom, dizzy and short of breath (Markowitz et al,
1989). Agoraphobia, generalised anxiety disorder (GAD), social phobia and phobias
of animals, heights, elevators, blood or injections are examples of other anxiety disorders (Ballenger, 2007; Craske et al, 1989; Magee et al, 1996; Schweizer, 1995). Due
to the varied character of anxiety disorders, concomitant conditions including stress,
diabetes, depression or hereditary factors could contribute to their aetiology (Amray
et al, 2019). Serotonin (5-hydroxytryptamine; 5-HT), GABA, noradrenaline (NE),
adrenocorticotropic hormone (ACTH), CRH, neuropeptide-Y and cholecystokinin
(CCK), main excitatory amino acid, glutamate, N-methyl-D aspartate (NMDA),
alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA) and kainic acid are
a few neurotransmitters involved in the development of anxiety. Serotonergic dysfunction leads to an aberrant 5-HT release and/or reuptake regulation or abnormal
5-HT signal response. A key stress-response mechanism that causes anxiety is the
LC noradrenergic system that releases epinephrine during stress and works in tandem with the corticotropin-releasing factor (CRF) system. CRF neurons are found in
the paraventricular nucleus, where they mediate the HPA axis’s activity in response
to stress, which raises plasma cortisol levels and increases CRF. The serotonergic
and noradrenergic systems are interconnected and together play a prime role in the
regulation of mood and anxiety (Bremner et al, 2010). The inhibitory neurotransmitter, GABA inuences the level of dopamine, 5-HT and NMDA. Thus, NMDA
antagonists and non-NMDA type receptors can reduce excitatory glutamate receptor activity and possess anxiolytic effects (LeDoux, 1994)). Alternately, increasing
GABA neurotransmission can reduce the output of the excitatory system. Thus, for
effective control of the behavioural and physiological responses related to anxiety,
a balance between NE, 5-HT, glutamate receptor-mediated excitement and GABA
receptor-mediated inhibition should exist. Selective 5-HT reuptake inhibitors (SSRI)
and 5-HT-norepinephrine reuptake inhibitors are the rst-line treatments for anxiety.
An alarming amount of people are becoming overly dependent on synthetic pharmaceuticals to treat or relieve anxiety disorders, yet there are still many people who
prefer herbal remedies. Important phytochemicals acting on the CNS are being identied, including saponins, alkaloids, polyphenols, triterpenes, essential oils, fatty
acids and avonoids. The phytoconstituents from families of herbs – Solanaceae,
Piperaceae, Hypericaceae, Plantaginaceae, Passioraceae, Araliaceae, Lamiaceae,
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Caprifoliaceae, Turneraceae, Elaeocarpaceae, Lamiaceae, Asteraceae and Apiaceae
are commonly used as anti-anxiety remedies. According to the European Medicines
Agency (EMA) and the National Agency of Sanitary Surveillance (ANVISA),
Withania somnifera L., Piper methysticum, Hypericum perforatum L., Bacopa
monnieri L., Passiora incarnata L. and Panax ginseng are safe herbal remedies.
Ocimum sanctum L. also known as Tulsi contains eugenol (70%) as a major constitu-
ent. Clinical study carried out in patients suffering from generalised anxiety disorder
were selected and given the ethanolic extract of Ocimum sanctum L. supplement
(500 mg capsule, twice daily) for 60 days. On completion of the study, reduced stress,
attenuated anxiety and negated depression attributing to the regulation of hypothalamohypophyseal-adrenocortical axis were noted (Bhattacharyya et al, 2008).
OciBest, an extract of Ocimum sanctum L, having ociglycoside-I (hydroxychavicol
glucoside/4-allyl-1-O-β-D-glucopyronosyl-2-hydroxybenzene; >
rinic acid (>0.2% w/w) and triterpene acids (>2.5% w/w) was tested in 158 patients
in a randomised, double-blind trial which exhibited antistress effects (Saxena et al,
2012). Eugenol treatment in rats exposed to restrain for 4 hours attenuated ulcer
index and reduced cortisol without affecting NE and amelioration of HPA axis
(Garabadu et al, 2011). The most commonly active phytoconstituents present in
Melissa ofcinalis L. (Lamiaceae) also known as lemon herb are rosmarinic acid,
ursolic acid and oleanolic acid is native to Europe and Asia and is responsible for its
antianxiety effect. Clinical investigation in patients with anxiety and sleep disorder,
supplemented with dried powder of aerial part of Melissa ofcinalis L. (3 g) for
56days showed improvement in anxiety score (Haybar et al, 2018). The author suggested its antianxiety effects attributed to its serotonergic activity, reduced cortisol
level and its GABA transaminase inhibitory effect. The preclinical study in rats
has proven that Melissa ofcinalis L. act by inhibiting GABA transaminase and
shows promising anxiolytic effect (Bathala et al, 2012). Hypericum perforatum L.
(Saint John’s Wort (SJW)) containing active phytoconstituents hypericin and hyperforin is majorly used in anxiety disorder. Hypericin inhibits monoamine oxidase-A
(MAO-A) and monoamine oxidase-B (MAO-B) enzymes and regulates dopamine
levels. Hyperforin elevates the extracellular levels of 5-HT, dopamine, NE, GABA
and L-glutamate. Passiora incarnata L. (Passion ower) contain active phytoconstituents such as orientin, isoorientin, vitexin, isovitexin and chrysin shows antianxiety effect by its action on benzodiazepine and GABA receptors (Table 5.1).
0.1% w/w), rosma-
5.4 PHYTOCONSTITUENTS USED FOR DEPRESSION
Depression is a neuropsychiatric disorder characterised by anxiety, aggression,
dementia and emotional imbalance. According to the World Health Organization,
depression is considered the most prevalent among all neuropsychiatric disorders.
Worldwide 322 million people are suffering from depression (Vasha et al, 2023).
Lack of diagnosis makes depression a more severe form, resulting in loneliness
and suicidal tendencies. Various studies have reported complications and comorbidities associated with depression such as cardiovascular changes, constipation,
colitis, erectile dysfunctions and thyroid problems. In severe cases, it may lead to
MDD, Alzheimer’s disease and diabetes. Various synthetic drugs such as tricyclic
Molecular Mechanism of Action of Phytoconstituents
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TABLE 5.1
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
Antipsychotic
1. Vitegnoside Vitex negundo
(Lamiaceae)
2. Bergenin Securinega virosa
(Euphorbiaceae)
3. Alkaloid, saponin
glycoside,
steroids, reducing
sugar, resin and
avonoid
4. Quercetin,
kaempferol
5. Saponins Crassocephalum
6. Flavonoids,
essential oils
7. Alpha lipoic acid Spinach/Spinacia oleracea
8. Silymarin Silybum marianum (L.)
9. Aleuronic acid Valeriana Ofcinalis L.
Albizia zygia (DC)
(Leguminosae-
Mimosoideae)
Lonchocarpus cyanescens
(Fabaceae)
bauchiense
(Asteraceae)
Ocimum sanctum
(Lamiaceae)
(Amaranthaceae), brocolli,
tomato
Gaertn
(Asteraceae)
(Valerianaceae)
Antagonizes
dopaminergic activity.
Antidopaminergic activity
on the melatonin MT1
and MT2 and promotes
sleep onset.
Enhance
glutamate and dopamine
release in the limbic
striatal regions.
Inhibition of
hyperactivation caused by
dopamine.
Blockade of
dopamine D-2 receptors
and GABAergic
activation
Decreases
dopamine levels and
reduces oxidative stress.
Restore
monoamines by
modulation of 5HT3
receptor.
Block the reuptake
of 5-HT into presynaptic
5-HT neurons.
GABA A receptor
modulator.
(Abidin et al,
2015; Ahmed
et al, 2014)
(Magaji et al,
2015)
(Amoateng et al,
2017; Kumbol
et al, 2018)
(Arowona et al,
2014)
(Taïwe et al, 2012)
(Sharma et al,
2016)
(Perera et al, 2011)
(Karcı and Celik,
2020)
(Karcı and Celik,
2020;
Kochlamazashvili
et al, 2010)
(Continued)
89
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NeuroPhytomedicine
TABLE 5.1
(Continued)
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
10. Morin Morus alba (Moraceae)
11. Mitragynine Mitragyna speciosa
(Rubiaceae)
12. Cannabidiol Cannabis sativa
(Cannabaceae)
Antidepressants
13. Curcumin
Chrysin
Arctigenin
Glycyrrhizic acid
14. Eugenol
Antiepilepsirine
Palmatine
Gallic acid
β-Carotene
Icariin
Fisetin
15. Cinnamic
aldehyde
Resveratrol
Salvianolic acid B
Ferulic acid
Quercetin
Curcuma longa L.
(Zingiberaceae)
Apis dorsata (Apidae)
Carthamus tinctorius L.
(Asteraceae)
Glycyrrhiza glabra L.
(Fabaceae)
Syzygium aromaticum
(Myrtaceae)
Albizzia julibrissin
(Fabaceae)
Berberis aristate
(Berberidiaceae)
Emblica ofcinalis
(Phylantheaceae)
Daucus carota subsp.
sativus (Apiaceae)
Epimedium grandiorum
(Berberidaceae)
Fragaria ananassa
(Rosaceae)
Cinnamomum verum
(Lauraceae)
Muscadine grapes
(Vitaceae)
Salvia miltiorrhiza
(Danshen)
Attenuate
neurochemical change
and reduce ROS.
Inhibit
dopamine-induced
contractile response.
Activates 5-HT1A
and glutamate receptor
(NMDA), inhibit FAAH
enzyme.
↓IDO/TDO
↓MAO-A
↓PG-E2
↓ TNF-α and IL-Iβ;
↑ Bcl-2 expression;
↓ NF-κB gene
expression.
(Ben-Azu et al,
2018)
(Vijeepallam et al,
2016)
(Xiang et al, 2022)
(Borges Filho et al,
2016; Seo et al,
2015; Temml et al,
2013; Wang et al,
2018)
(Tao et al, 2005)
(Yao et al, 2015)
(Continued)
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91
TABLE 5.1
(Continued)
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
16. Withaferin-A,
withanolide
17. Asiatic acid,
madecassic acid,
asiaticoside,
madecassoside
and brahmic acid
18. Baicalin and
wogonin
19. Carnosine,
carnosic acid,
carnosal,
rosmanol,
epirosmanol
(Lamiaceae)
Pavetta owariensis
(Rubiaceae)
Coccinia indica
(Cucurbitaceae)
Antistress
Withania somnifera
(Solanaceae)
Centella asiatica L.
(Apiaceae)
Scutellaria baicalensis
(Lamiaceae)
Rosmarinus ofcinalis
(Lamiaceae)
↓ ACTH and CORT;
↑ CAT, SOD and GSH
peroxidase activities;
↓ MDA; ↓ IL-6, IL-1β
and TNF-α; ↓ NLRP3
inammasome activation.
↓ IL-1β, IL-6 and
TNF-α; ↓ ACTH and
CORT; ↓ NF-κB
activation; ↓ nNOS
expression; ↑ IL-10; GR
protein expression.
↑ GSH; ↑ SOD and CAT
activity; ↑ 5-HT; ↓ Glu;
↓ IL-1β and TNF-α.
Reduction of
cortisol levels.
Increase
upregulates receptor
population in corpus
striatum.
Decrease
oxidative stress.
Antioxidative
activity, interact with
GABA receptor, reduce
serum levels of IL-2,
corticosterone.
Modulate
sympathetic nervous
system and HPA axis,
activate cholinergic activity
(AchE activity) in PC12
cells via phosphorylation
of ERK1/2.
(Archana and
Namasivayam,
1998; Jamalludin
and Manshoor,
2022)
(Zakaria et al,
2023; Kalshetty
et al, 2012)
(Lee et al, 2007)
(Kayashima et al,
2020)
(Continued)
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NeuroPhytomedicine
TABLE 5.1
(Continued)
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
20. Ginsenoside Rb1
and Rg3
21. L-Theanine Camellia sinensis
22. Rosalin (WS®
1375), Rodiolin,
rosin, rosavin,
rosarin and
rosiridin
23. Apigenin Matricaria recutita
24. Rosmarinic acid Melissa ofcinalis
25. Rosmarinic acid
triterpenoids,
ursolic acid
oleanolic acid
26. Triterpenes,
derivatives of
avones
27. Linalool and
linalyl
acetate
Panax ginseng
(Araliaceae)
(Theaceae)
Rhodiola rosea
(Crassulaceae)
(Asteraceae)
(Lamiaceae)
Antianxiety
Melissa ofcinalis
(Lamiaceae)
Cimicifuga pregula L. Nutt
(Ranunculaceae)
Lavandula angustifolia
Mill. (Lamiaceae)
Increased ACTH
and corticosterone.
Reduce
presynaptic glutamate
release, increase inhibitory
neurotransmitter GABA
and enhance glycine and
dopamine release.
Normalise cortisol
synthesis.
Afnity for
benzodiazepine receptors,
binds to GABA receptors,
reduces the levels of the
stress-induced ACTH.
Inhibits GABA
transaminase activity and
slow the degradation of
GABA.
Inhibitor of rat brain
GABA transaminase.
Inhibited the
oxidative stress.
Act in the
hypothalamus
vasomotor centre,
dopaminergic action.
Anxiolytic-like
effect through 5-HT1A
receptors.
(Huang et al,
2019)
(Sarris et al, 2019;
Unno et al, 2013)
(Emilija and
Quintela, 2022)
(Ebrahimi et al,
2022)
(Wang et al, 2022)
(Heydari et al,
2019)
(Fajemiroye et al,
2016)
(López et al, 2017)
(Continued)
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93
TABLE 5.1
(Continued)
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
28. Hypericin,
hyperforin
29. Linalool and
β-pinene
30. Methyl isoeugenol
and oleanolic acid
31. Mesembrine,
mesembranol,
mesembrenol and
mesembrenone
32. Bacopasides Bacopa monnieri
33. Benzo-avonoids Passiora incarnate
34. Eleutherosides,
sennosides
Hypericum perforatum L.
(Hypericaceae)
Litsea glaucescens
(Lauraceae)
Pimenta
pseudocaryophyllus
(Gomes), ChamguavaL. R.
Landrum
(Myrtaceae)
Sceletium tortuosum
(Aizoaceae )
(Scrophulariaceae)
(Passioraceae)
Eleutherococcus senticosus
(Araliaceae)
Selective
inhibitor of MAO-A and
MAO-B Inhibition of
5-HT, NE and DA
uptake; antagonist of
NMDA receptors;
moderate interactions
with the GABA A
receptor, Suppression of
the release of
interleukin.
Interaction with
the serotonergic 5-HT1A
receptors, a2- and
b-adrenoceptors and
dopaminergic receptors
D1.
Acts on 5-HT1A
receptor.
Inhibitory
effects on 5-HT reuptake,
binds to gamma butyric
acid (GABA).
Lower
susceptibility to stress
even before exposure.
Acts on
benzodiazepine and
GABA receptors, MAO
enzyme inhibiting
properties.
HPA axis
regulation.
(Oliveira et al,
2016)
(Guzmán-
Gutiérrez et al,
2015)
(Fajemiroye et al,
2016)
(Carpenter et al,
2016)
(Calabrese et al,
2008;
Sathyanarayanan
et al, 2013)
(Dhawan et al,
2001)
(Lee and Rhee,
2017)
(Continued)
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NeuroPhytomedicine
TABLE 5.1
(Continued)
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
35. Ethanol extract of
ower
36. Ginsenoside Rb1 Panax ginseng
37. Hydroalcoholic
extract
38. Ginkgolide-A Ginkgo biloba
39. Baicalin, baicalein Scutellaria lateriora
40. Valerenic acid,
valepotriates
41. Mother tincture Turnera aphrodisiaca
42. Riparin III Aniba riparia
43. Hydroethanolic
extract of the
aerial part
44. Clary (aromatic
essential oil)
45. Root tincture Artemisia vulgaris
Echium amoenum
(Boraginaceae)
(Araliaceae)
Salvia reuterana
(Lamiaceae)
(Ginkgoaceae)
(Lamiaceae)
Valeriana ofcinalis L.
(Caprifoliaceae)
(Passioraceae)
(Lauraceae)
Aloysia polystachya
(Verbenaceae)
Salvia sclarea
(Lamiaceae)
(Asteraceae)
Reduce
oxidative stress and
elevation of
catecholamine levels.
Modulate
monoamine
neurotransmitter system,
regulate the expression of
neurotrophic factors,
regulate HPA axis
function, antiinammatory action.
Acetylcholinesterase
inhibitor, GABA receptor
agonist.
Regulate
dopamine, 5-HT and
inammatory glialderived proteins.
GABAA agonist
GABAA agonist
GABA agonist
Monoamine
inhibition
Selective 5-HT
reuptake inhibition.
Modulation of
the dopaminergic
pathway.
GABAA receptor
modulation.
(Nouri et al, 2019)
(Bui et al, 2022)
(Rabbani et al,
2005)
(Deravi, 2022)
(Awad et al, 2003)
(Murphy et al,
2010)
(Kumar et al,
2008)
(Sousa et al, 2004)
(Carmona et al,
2019)
(Seol et al, 2010)
(Hernandez-Leon
et al, 2017; Khan
et al, 2016)
(Continued)
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95
TABLE 5.1
(Continued)
Summary of Phytoconstituents Reported for Various Neuropsychiatric
Disorders and Their Mechanism of Action.
S. No Antipsychotic Biological Source-Family Molecular Mechanism References
46. Rutin Camellia sinensis (L.)
Kuntze
(Theaceae)
47. Quercetin Chenopodium album
(Amaranthaceae)
48. Kaempferol,
quercetin
alkaloid and
avonoid
49. Honokiol Magnolia obovata
50. Eugenol,
1,8-cineole,
1,8-bisabolene
Sansevieria trifasciata
(Asparagaceae)
Ginkgo biloba
(Ginkgoaceae)
Elaeocarpus ganitrus
(Elaeocarpaceae )
(Magnoliaceae)
Ocimum sanctum
(Lamiaceae)
GABAA
receptors modulation.
Modulation of
GABAergic and
serotonergic system.
Modulation of
molecular pathways such
as NF-kB, PI3k/AKT,
MAPK, Bcl2, Caspase 3
and VEGF.
Effects on
GABA-benzodiazepine
receptor, inhibitory
activity on inammatory
mediator.
Regulation of HPA
axis
(Hernandez-Leon
et al, 2017)
(Cárdenas-
Rodríguez et al,
2014)
(Kim et al, 2013)
(Ham et al, 2020)
(Bhattacharyya et
al, 2008)
51. Linalool and
linalyl acetate
52. Apigenin Matricaria recutita
53. Linalool,
γ-terpinene,
α-pinene
Abbreviations: Corticotropin-releasing hormone (CRH), dopamine (DA), nor-epinephrine (NE),
5- hydroxytryptamine (5-HT), gamma-aminobutyric acid (GABA), N-methyl-D-aspartate
(NMDA), monoamine oxidase (MAO), hypothalamic–pituitary–adrenal (HPA) axis, corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), reactive oxygen species
(ROS), acetylcholinesterase (AchE), fatty acid amide hydrolase (FAAH), tryptophan-2,3dioxygenase (TDO), indole 2,3 amine dioxygenase (IDO), superoxide dismutase (SOD), catalase
(CAT), tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), nuclear factor kappa b
(NF-kb), mitogen-activated protein kinase (MAPK).
Lavandula angustifolia
Mill. (Lamiaceae)
Coriandrum sativum
(Apiaceae)
(Asteraceae)
Cortical sparing
effect.
Effect on
5-HT1A receptor.
Ligand for the
central benzodiazepine
receptors.
MAO-B
inhibition.
(Caputo et al,
2018)
(Viola et al, 1995)
(Hosseini et al,
2021)
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