Herbal plants: A boon in the treatment of Asthma
Salman D Shaikh, Gorakshanath M Rahane, Akshay B Gakedar, Habeeba S Shaikh
Department of Pharmacy, Matoshri Institute of pharmacy Dhaonre Yeola Maharashtra India.
*Corresponding Author E-mail: habibashaikh762@gmail.com
ABSTRACT:
Asthma is a common disease that is increasing in prevalence worldwide with the highest prevalence in industrialized countries. Asthma affects around 300 million people worldwide, with more than 100million expected to be affected by 2025. From prehistoric times, plants have been excellent sources of medicine. As current asthma therapy is unsatisfactory due to side effects, many people are turning to complementary and alternative medicine to treat their asthma. Plants are mentioned in Ayurveda and other Indian literature to treat a variety of human ailments. There are around 45000 plant species in India, with thousands of them claiming therapeutic benefits. Recent studies on herbs mentioned in ancient literature or used traditionally for asthma have shown antiasthmatic, antihistaminic, and antiallergic properties. According to this review, various plants and their extracts have antiasthmatic, antihistaminic, anticholinergic, and anti- allergic properties.
KEYWORDS: Asthma, Pathophysiology, Inflammatory mediators, Anti-asthmatic plant, Herbal medicine,
INTRODUCTION:
Asthma is a long-term inflammatory condition of the lungs that frequently results in wheezing, shortness of breath, chest tightness, and coughing, especially at night and in the morning. The majority of the time, these symptoms are linked to widespread but variable bronchoconstriction and airflow limitation that is at least partially reversible, either naturally or with therapy. The symptoms of disease include increased mucus secretion, inflamed bronchial walls, and increased airway responsiveness to various triggers, which results in episodic bronchoconstriction. In individuals with normal airways, some of the stimuli that cause attacks in patients would have little to no impact.
Numerous cells, including lymphocytes, eosinophils, mast cells, macrophages, neutrophils, and epithelial cells, are involved in the immune reaction. eople who have asthma go through different severity that cause bronchospasm, dyspnea, coughing, and wheezing1. Rarely, a condition known as status asthmaticus, which is characterized by persistent attacks, proves fatal; these patients typically have a lengthy history of asthma. Patients may experience practically no symptoms in between attacks. In the past forty years, there has been a marked rise in the prevalence of asthma in the Western world. Asthma may be categorized into atopic (evidence of allergen sensitization, often in a patient with a history of allergic rhinitis, eczema) and non-atopic (without evidence of allergen sensitization). In either type, episodes of bronchospasm can be triggered by diverse mechanisms, such as respiratory infections (especially viral infections), environmental exposure to irritants (e.g., smoke, fumes), cold air, stress, and exercise. Recent studies have suggested that the recognition of sub phenotypes of asthma based on the pattern of airway inflammation may also be useful. Different patterns of airway inflammation, including eosinophilic, neutrophilic, mixed, and pauci-granulocytic asthma are being supported by increasing data. These subsets may vary in terms of immunopathology, etiology, and therapeutic response. Another way to categorize asthma is by the things or situations that cause bronchoconstriction. These include asthma that is cyclical, exercise-related, drug-induced (e.g., aspirin-induced), occupational, and smokers asthmatic bronchitis1.
TYEPS OF ASTHMA |
Atopic asthma |
Non atopic Asthma |
|
Drug induced Asthma |
|
Occupational Asthma |
This most common type of asthma is a classic example of type I IgE-mediated hypersensitivity reaction. The disease usually begins in childhood and is triggered by environmental allergens, such as dusts, pollens, roach or animal dander, and foods. A positive family history of asthma is common, and a skin test with the offending antigen in these patients results in an immediate wheal-and-flu are reaction. Atopic asthma may also be diagnosed based on evidence of allergen sensitization by serum radioallergosorbent tests (called RAST), which identify the presence of IgE specific for a panel of allergens1.
2) Non-Atopic Asthma:
The second group of individuals with asthma does not have evidence of allergen sensitization, and skin test results are usually negative. A positive family history of asthma is less common in these patients. Respiratory infections due to viruses (e.g., rhinovirus, parainfluenza virus) are common triggers in non-atopic asthma. In these patients hyperirritability of the bronchial tree probably underlies their asthma. It is thought that virus-induced inflammation of the respiratory mucosa lowers the threshold of the sub epithelial vagal receptors to irritants. Inhaled air pollutants, such as sulfur dioxide, ozone, and nitrogen dioxide, may also contribute to the chronic airway inflammation and hyper reactivity that are present in some cases1.
3) Drug-Induced Asthma:
Several pharmacologic agents provoke asthma. Aspirin-sensitive asthma is an uncommon yet fascinating type, occurring in individuals with recurrent rhinitis and nasal polyps. These individuals are exquisitely sensitive to small doses of aspirin as well as other nonsteroidal anti-inflammatory medications and they experience not only asthmatic attacks but also urticaria. It is probable that aspirin triggers asthma in these patients by inhibiting the cyclooxygenase pathway of arachidonic acid metabolism without affecting the lipoxygenase route, thus tipping the balance toward elaboration of the bronchoconstrictor leukotrienes1.
4) Occupational Asthma:
This form of asthma is stimulated by fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene), and other chemicals (formaldehyde, penicillin products). Minute quantities of chemicals are required to induce the attack, which usually occurs after repeated exposure. The underlying mechanisms vary according to stimulus and include type I reactions, direct liberation of bronchoconstrictor substances, and hypersensitivity responses of unknown origin1.
PATHOPHYSIOLOGY:
The pathological feature of bronchial asthma is the infiltration of eosinophils into the lung submucosa. It is thought that eosinophil activation, which causes the release of a variety of highly charged cytotoxic cationic proteins like major basic protein is a key factor in the aetiology of this illness by causing harm to the airway epithelium1. The pathophysiology of asthma includes the occurrence of acute and chronic inflammation that causes vascular permeability to increase, edoema to form and smooth muscle contraction of the airways to narrow the airways2,3. Atopy, a genetic predisposition to type I hypersensitivity, and exposure to poorly understood environmental triggers are the primary causes of atopic asthma. According to the theory, inheriting susceptibility genes predisposes people to having strong TH2 reactions to environmental antigens (allergens) that are typically overlooked or cause harmless reactions in most people. Initial sensitization to inhaled allergens causes TH2 cells to be induced, which sets the stage for the response in the airways. The cytokines that are released by TH2 cells encourage allergic inflammation and prompt B cells to make IgE and other antibodies. These cytokines include IL-4, which stimulates the production of IgE; IL-5, which activates locally recruited eosinophils; and IL-13, which stimulates mucus secretion from bronchial submucosal glands and also promotes IgE production by B cells. As in other allergic reactions, IgE coats submucosal mast cells, and repeat exposure to the allergen triggers the mast cells to release granule contents and produce cytokines and other mediators, which collectively induce the early-phase (immediate hypersensitivity) reaction and the late-phase reaction. The early reaction is dominated by bronchoconstriction, increased mucus production, and variable degrees of vasodilation with increased vascular permeability. Bronchoconstriction is triggered by direct stimulation of subepithelial vagal (parasympathetic) receptors through both central and local reflexes (including those mediated by unmyelinated sensory C fibers4. The late-phase reaction consists largely of inflammation with recruitment of leukocytes, notably eosinophils, neutrophils, and more T cells. Leukocyte recruitment is stimulated by chemokines produced by mast cells, epithelial cells and T cells, and by other cytokines. Epithelial cells are known to produce a large variety of cytokines in response to infectious agents, drugs and gases as well as to inflammatory mediators. This second wave of mediators stimulates the late reaction. For example, eotaxin, produced by airway epithelial cells, is a potent chemo attractant and activator of eosinophils. The major basic protein of eosinophils, in turn, causes epithelial damage and more airway constriction. Many mediators have been implicated in the asthmatic response, but the relative importance of each putative mediator in actual human asthma has been difficult to establish. The long list of “suspects” in acute asthma can be sub classified by the clinical efficacy of pharmacologic intervention with inhibitors or antagonists of the mediators5,6,7.
FUTURE PERSPECTIVE OF HERBAL DRUG IN ASTHMA:
About 90% of the most recent pharmaceutical discoveries are still derived from traditional medicine and medicinal herbs in general. Over 80% of the world's population continues to receive health care from traditional medicine, particularly in developing nations. Living instances of drug discoveries from the past and present abound, including those for anticancer, antiasthma, anti-diabetic, antihypertensive, and many other conditions that have their roots in conventional medicine. Numerous plants can be extensively cultivated for regional commercial production of pharmaceuticals and herbal dietary supplements8. It is important to make sure that what is understood is put to good use for both monetary gain and the improvement of our population's health. Establishing the required expertise for traditional medicine development and making conscious efforts to promote local industrial production of traditional/herbal medicines should be done to enable cultivation and thereby aid in the alleviation of poverty9,10.
NATURAL REMEDIES FOR THE TREATMENT OF ASTHMA:
It has been extensively reported through ethno pharmacological studies that using natural products to treat physiologic disorders, particularly in combination with other medications, is an essential scientific tool for discovering novel bioactive compounds from natural sources. Drugs from natural sources continue to make significant contributions to the discovery and production of new medicines despite the significant scientific advancements in chemical and pharmaceutical technology for the synthesis of new molecules. ESE studies are initially founded on the conventional use of natural products, which attracts the interest of pharmaceutical companies because of their practicality and affordability, enabling the companies to carry out numerous studies assessing their therapeutic activities, toxicity and safety. Additionally, using natural remedies as an additional form of treatment is crucial. In the World, the use of natural products vitamins and other dietary supplements as auxiliary treatments represent about 70% of the conventional therapies among the diseases that natural products are used for those of allergic and inflammatory character can be highlighted. In fact, according to the literature, the alternative medicine associates the use of these products with biochemical mechanisms involved in immunomodulation, which can contribute to the management of these diseases use of plant-based products for asthma treatment has been reported by the traditional medicine for over 5000 years, since, the use by the Chinese culture of the infusion of Ephedra sinica, which is as an immune system stimulator able to decrease asthma crises. More recently, a study performed by Costa and colleagues described the main natural sources for the treatment of asthma used by the Brazilian families from the Northeast region of the country study included beet, honey, onion, lemon, garlic, yarrow, and mint, demonstrating the wide variety of natural products used on asthma treatment in children .Additionally, other natural-derived products have been widely cited in asthma treatment, such as natural oils from plants and animals, which can be obtained by different extraction process. Plant-derived natural oils represent the main natural products used on the complementary asthma therapy due to the presence of compounds such as phenylpropanoids and mono- and sesquiterpenes as the major bioactive compounds, which provide their anti-inflammatory, antifungal, antibacterial, and anesthetic properties11.
BRIEF REVIEW OF ANTIASTHMATIC PLANTS:
Table 1.Diffrent plants part effective in treatment of asthma
Name of plant |
Family |
Part used |
Chemical constituents |
Mechanism of action |
Reference |
Abies webbiana Lindl. |
Pinaceae |
Leaves |
1-(4'-methoxyphenyl)-aziridine |
Mast cell stabilizer |
2,12,13,14 |
Allium cepa |
Liliaceae |
Bulb |
Quercetin |
1. Mast cell stabilizer 2. Lipoxygenase inhibitor 3. PAF inhibitor3 4. COX inhibitor |
2,12 ,13 |
Achyranthes aspera |
Amaranthaceae |
Fruit |
Saponin C Saponin D |
Mast cell stabilizer |
2,15,16 |
Albizzia lebbeck |
Leguminosae |
Bark |
Alkaloids, tannins, flavonoidsv |
1. Bronchodilator 2. Mast cell stabilizer |
2,13,12 |
Achillea mellifolium |
Asteraceae (compositae) |
Flower |
Alkaloids |
Inhibits action of histamine, acetylcholine and 5-HT |
2,9,10 |
Asystasia gangetica |
Acanthaceae |
Leaves |
Triterpenoids, saponins, Steroidal aglycone |
1. Bronchodilator 2. Anti-inflammatory |
2,13 |
Acorus calamus |
Araceae |
Rhizome |
Asarone |
Inhibits action of histamine, acetylcholine and 5-HT |
5,17,18 |
Ammi visnaga |
Umbelliferae |
Seeds |
Khellin |
Bronchodilator |
2,19 |
Adhatoda vasica |
Acanthaceae |
Leaves |
Vasicinol, vasicine |
Bronchodilator |
21 |
Boswellia serrata |
Burseraceae |
Root |
Boswellin, Boswellic acid |
Inhibits leukotriene biosynthesis |
2,19 |
Balanites roxburghii |
Simarubaceae |
Stem bark |
Alkaloids |
1. Bronchodilator 2. Mast cell stabilizer |
2,20 |
Cedrus deodara |
Pinaceae |
Wood |
Himacholol |
Mast cell stabilizer |
2,16 |
Curculigo orchioides |
amarylliaceae |
Rhizomes |
Triterpenoids sapogenins and saponin glycosides |
1. Antihistaminic 2. Anti-inflammatory |
5,13 |
Clerodendron phlomidis |
Verbenaceae |
Leaves |
Flavonoids, terpenoids, steroids |
1. Antihistaminic 2. Mast cell 3stabilizer |
2,10 |
Curcuma longa |
Zingiberaceae |
Rhizome |
Curcuminoids |
nhibits histamine release |
5,15,16 |
Cassia sophera |
Caesalpiniaceae |
Leaves |
Flavonoids, glycosides |
1. Bronchodilator 2. Antihistaminic 3. Antiallergic 4.anti-inflammatory |
2,13,14,19 |
Centipeda minima |
Compositae |
Whole plant |
Pseudoguainolide, sesquiterpene, lactone, flavonoids |
Antiallergic |
2,13 |
Ephedra gerardiana |
Ephedraceae |
Stem |
Ephedrine |
Bronchodilator |
5,16 |
Eucalyptus globules |
Myrtaceae |
Leaves |
Volatile oil |
Anti-inflammatory |
2,20 |
Echinodorus scaber |
Alismataceae |
Leaves |
Vitexin,rutin,and galli cacid |
Decrease the migration of inflammatory cells and reduce the Th2 cytokines |
2,14 |
Aegle marmelos |
Rutaceae |
Leaves |
Alkaloid-aegeline |
Antihistaminic |
5,15 |
Hedychium spicatum |
Zingiberaceae |
Rhizome |
Sitosterol, Volatile oil |
Anti-inflammatory |
2,13,14 |
Glycyrrhiza glabra |
Leguminosae |
Root |
Glycyrrhizinic acid |
1.Antihistaminic 2.Antiallergic |
2,12 |
Inula racemosa |
Asteraceae |
Root |
Inulin, sesquiterpene lactone alantolactone |
Antihistaminic |
5,17,18 |
Moringa oleifera |
Morangaceae |
Seed |
Tannins, steroids, triterpenoids, 3flavonoids,alkaloids, saponins |
Antihistaminic |
2,12,13 |
Myrica sapida |
Myricaceae |
Bark |
Glycosides |
Mast cell stabilizer |
2,12,20 |
Nigella sativa |
Ranunculaceae |
Seed |
Volatile oil, fatty acid |
Bronchodilator |
2,12,20 |
Ocimum sanctum |
Labiateae |
Leaves |
Ursolic acid |
Mast cell stabilizer |
5,18 |
Picorrhiza kurroa |
Scrophulareaceae |
Roots |
Picorrhizin |
Antihistaminic |
3,12,19 |
Lipidum sativum |
Cruciferae |
Seeds |
Alkaloids, Flavonoids |
Bronchodilator |
2,13,14 |
Passiflora incarnat |
Passifloraceae |
Leaves |
Benzoflavone |
Bronchodilator |
2,10,13 |
Solanum xanhocarpum |
Solanaceae |
Flowers |
Phyto-sterol, alkaloids, flavonoooids, Steroids |
1. Antihistaminic 2. Mast cell stabilizer |
5,17 |
Terminalia belerica |
Combrataceae |
fruits |
Beta sitosterol, Gallic acid, ellagic acid, glycoside |
Mast cell stabilizer |
2,15,19 |
Tinospora cordifolia |
Mensipermaceae |
Stem |
Alkaloids |
1. Antihistaminic 2. Mast cell stabilizer |
2,19,20 |
Tamarindus indica |
Caesalpiniaceae |
leaves |
Flavone, Glycosides |
1. Brochodialator 2. Antihistaminic 3. Anti-inflammatory |
5,16,17 |
Tussilago farfara L |
Asteraceae |
Root and leaves |
1-nonene (40.1%), α-phellandrene (26.0%) and ρ-cymene |
by inhibiting arachidonic acid metabolism and nitric oxide (NO) production in lipopolysaccharide-activated macrophages. |
2,17,18 |
Vanda spacthulata Species. |
Orchidaceae |
Flower |
Beta sitosterol |
By inhibiting MoA enzyme |
5,15,16 |
Vepris bilocularis Engler |
Rutaceae |
Wood |
methyl epi-isoobacunoate |
Not identified yet |
2,19,15 |
Verbascum thapsus L |
Scrophulariaceae |
Whole plant |
iridoid, flavonoids, saponins, monoterpene glycosides, phenylethanoid glycosides, neolignan glycosides, steroids and spermine alkaloids |
Antiviral activity against the pseudorabies virus strain RC/79 (PrV), and also for its cytotoxic activity on Vero cells. |
2,12,13 21 |
Pie1 Representing Statistics of different type of medicinal plants part used for the treatment of Asthma.
CONCLUSION:
Herbal medicine has been used as one of the oldest forms of remedies utilized by humans. From the above study we conclude that plants play an important role in treatment of Asthma in across all over the World. Synthetic drugs are effective against Asthma but they have numerous side effects, so plants are the cheapest and safest role in treatment of Asthma.
REFERENCE:
1. K. Abbas, Aster Robbins and Cotran. Pathologic Basis of Disease Published by Elsevier, vol 2, 679 to 682.
2. R. N. Kale, R. N. Patil and R. Y. Patil. Asthma and herbal drugs. International Journal of Pharmaceutical Sciences and Research, 2010; 12(1): 975-8232
3. K.D Tripathi. Essential of Medical Pharmacology, Jaypee Publication, Edition 8th, 2019:237 to 254
4. Larché M, Akdis CA, Valenta R. Immunological mechanisms of allergen-specific immunotherapy. Nat Rev Immunol. 2006; 6 (10): 761–771
5. S. Azman, M. Sekar, et al. Traditional Medicinal Plants Conferring Protection against Ovalbumin-Induced Asthma in Experimental Animals. J Asthma Allergy. 2021; 14: 641–662
6. Lambrecht, B.N.; Hammad, H.; Fahy, J.V. The Cytokines of Asthma. Immunity. 2019, 50, 975–991.
7. G. Kaufman Asthma: pathophysiology, diagnosis and management. Nurs Stand. 2011; 26(5):48.
8. M.A Lyengar, Jambaiah KM, Rao GM. Studies on an anti-asthma kada: A Proprietary Herbal Combination Part-I Clinical Study. Indian Drug. 1994; 31(5):183–186.
9. Brusselle, G.G.; Koppelman, G.H. Biologic Therapies for Severe Asthma. N. Engl. J. Med. 2022, 386, 157–171.
10. S. Tarek. Towards a deep understanding of bronchial asthma. Egyptian Journal of Bronchology. 2007; 1(1):120-124.
11. L. Amaral-Machado, et al. Use of Natural Products in Asthma Treatment. Hindawi Evidence-Based Complementary and Alternative Medicine. 2020: 35
12. S. Tarek. Towards a deep understanding of bronchial asthma. Egyptian Journal of Bronchology, 2007; 1(1):120-124.
13. A.Sharma Shanker C, Tyagi L, Singh M, Rao CV. Herbal medicine for market potential in India: An Overview. Academic Journal of Plant Sciences. 2008; 1(2): 26-36.
14. Rajani GP, Patil UA, Deb J. Anti-asthmatic an overview Indian Drugs 2006; 43(10):781-89.
15. D. Kumar, S. Bhujbal, R. Deoda, and S. Mudgade. Bron-chodilator activity of aqueous extract of stem bark of ai-lanthus excelsaroxb, Pharmacognosy Research. 2010; 2(1): 102–106, 2010.
16. T. T. Oliveira, K. M. Campos, A. T. Cerqueira-Lima et al., Potential therapeutic effect of Allium cepa L. and quercetinn a murine model of Blomia tropicalis induced asthma, DARU Journal of Pharmaceutical Sciences. 2015; 23(1):18.
17. M. E. Houssen, et al. Natural anti-inflammatory products and leukotriene inhibitors as complementary therapy for bronchial asthma, Clinical Biochemistry. 2010; 43(10): 887–890.
18. J. Mlcek, T. Jurikova, S. Skrovankova, and J. Sochor. Quercetin and its anti-allergic immune response. Molecules. 2016; 21: 623–638.
19. Sundeep SS, Mamudipudi TK, Anthony PS, Stephen TH. The anti-inflammatory effects of leukotriene-modifying drugs and their use in asthma. Chest. 2001; 119:1533-1546.
20. Doshi U, Salat P, Parikh V. Cytokine modulators in Asthma: clinical perspectives. Indian J Pharmacol. 2002; 34: 16-25.
21. Amos S, Gamaniel K, Akah P, Wambebe C. Anti-inflammatory and muscle relaxant effect of aqueous extract of Pavetta crassipes leaves. Fitoterapia. 1998; 69:425–429.
Received on 10.08.2023 Modified on 09.10.2023
Accepted on 19.11.2023 ©A&V Publications All right reserved
Res. J. Pharmacognosy and Phytochem. 2024; 16(1):47-51.
DOI: 10.52711/0975-4385.2024.00010