Cascabela Thevetia: The Toxic Beauty of Yellow Oleander

Yellow oleander/ Cascabela thevetia / কল্কে ফুল (Bengali)/ Pili Kaner(Hindi)

General features: Cascabela thevetia (CT), commonly called Yellow oleander, is a highly toxic tropical flowering plant in the family Apocynaceae (dogbane) and the genus Cascabela. Its toxicity has been compared with rattlesnake venom [1,2] and is chiefly attributed to the powerful cardiac glycosides thevetin A and B, which can interfere with normal heart function [3]. CT commonly grows in dry regions, open woodlands, gardens, and along roadsides. Although it has been used in traditional medicine for various ailments, its high toxicity remains a serious concern. The plant’s white latex sap is also highly poisonous because it contains several toxic phytoconstituents. Yellow oleander/CT is sometimes called the “suicide tree” because of past clusters of intentional self-poisoning, notably in Sri Lanka in the 1980s [https://doi.org/10.1046/j.1365-3156.1999.00397.x]. One reported episode involved two village girls in northern Sri Lanka who died after eating CT seeds following a family dispute. Later investigations suggested that such cases could spread through social contagion, a pattern also observed in rural Indian villages where CT is commonly grown in household yards. Over several decades, CT became recognized as a public health hazard, with similar incidents reported in India and other Southeast Asian countries, particularly among young adults in rural areas. Between 2000 and 2020, social media and the internet further amplified the plant’s dangerous reputation worldwide. Its easy availability and ornamental appeal also increase the risk of sporadic accidental poisoning.

Ingesting the leaves or seeds of Cascabela thevetia can cause a burning sensation in the mouth, nausea, vomiting, abdominal cramps, diarrhea, dizziness, life-threatening arrhythmias, and severe bradycardia that markedly slows the heartbeat [4]. Its milky sap may irritate the skin and eyes and cause severe dermatitis, and smoke from burning the plant is also highly toxic [5]. The plant produces attractive bright yellow or white trumpet- to funnel-shaped flowers. In Bengali, Cascabela thevetia is commonly known as Kolke flower (কল্কে ফুল) and is frequently used in Hindu religious rituals, especially Shiva Puja. Although native to Mexico and Central America, CT is now widely cultivated as an ornamental plant and is often seen in temple yards across India. The name Cascabela comes from the Spanish cascabel, meaning the rattle of a snake, particularly a rattlesnake, reflecting the plant’s extreme toxicity. The species name thevetia honors André de Thevet (1516–1590 AD), a French Franciscan priest who encountered the plant in South America during his expedition to Brazil. Drought-, salt-, and heat-tolerant, CT thrives in full sun and well-drained soil. In tropical cities, it is commonly planted along roadsides, beaches, and lakesides for shade. This multi-branched shrub grows 10 to 20 feet tall and develops a dense canopy. Its narrow, linear-lanceolate leaves are about 6 inches long, glossy bright green above, and have rolled-under margins. When cut or broken, the plant releases a poisonous milky-white latex. Its fragrant, usually bright yellow flowers appear in clusters at branch tips from spring to autumn, though creamy-white cultivars are sometimes found. The conspicuous lantern-shaped, angular fruits have soft flesh and contain two to four large, hard seeds [5].

History of CT: In India, CT flowers are widely offered in worship of Lord Shiva, which explains the plant’s frequent presence in temple yards across the country. Although native to tropical regions of South and Central America, CT was introduced to India during the colonial era as an ornamental garden plant valued for its elegant, bright yellow, trumpet-shaped, fragrant flowers. Because of its exceptional drought and heat tolerance, it adapted readily to India’s tropical climate. Despite its serious toxicity, Hindu devotees continue to use the flowers in religious offerings, especially to Lord Shiva. Practitioners of traditional and folk Indian medicine also occasionally prescribe highly diluted preparations for conditions such as ringworm, fever, wound healing, jaundice, purgative, and tumors. In the late 20^th century, CT gained attention as a public health concern because it grows in many public and residential spaces, including backyards and temple yards, where it is used in daily Shiva Puja rituals. Its toxic seeds can cause accidental poisoning in children. Although adults in remote areas are generally aware of the danger, no regulation has yet been adopted to control its growth and better protect children [6].

Phytochemical components and their reactivities: Chemical analysis of the CT plant shows the following major categories of bioactive phytochemicals, totaling almost 81. The most common and abundant are cardenolides/cardiac glycosides, which are highly toxic and pharmacologically important for numerous therapeutic uses.

Category	Major Phytochemicals
Cardenolides/ Cardio glycosides	Thevetin A & B, Neriifolin, Peruvoside, Oleandrin, Ruvoside, Thevetoxin, and several others.
Terpenoids	Ursolic acid, Oleanolic acid, Lupeol acetate, Neolupenyl acetate, β-sitosterol, Stigmast-5-en-7-one, iridoid glucosides, and others of the similar category.
Phenolics and flavonoids	Quercetin, Kaempferol, Coumarins, polyphenols, and tannins.
Other active chemicals	Alkaloids, Saponins, Quinones, and Phlobotannins.

It is widely known that CT contains diverse bioactive phytochemicals in its leaves, bark, roots, fruits, flowers, and seeds, including cardiac glycosides, alkaloids, flavonoids, steroids, terpenoids, tannins, and saponins. The milky latex released when its branches or leaves are broken is highly toxic and contains numerous bioactive compounds, especially cardenolides/cardiac glycosides such as thevetin A and B, neriifolin, peruvoside, ruvoside, and thevetoxin. It also contains cysteine peptidase, carbohydrates, lignans, tannins, coumarins, and volatile oils [7]. Thevetins inhibit Na+/K+-ATPase on myocardial cell membranes by binding to the enzyme’s extracellular domain, thereby blocking normal ion transport: the influx of two K+ ions and the efflux of three Na+ ions. This raises intracellular Na+ levels and disrupts the Na+/Ca+2 exchanger, which normally removes Ca+2 from cells. The resulting calcium overload in the myocardial sarcoplasmic reticulum and cytoplasm causes excessive cardiac contractility, alters the resting potential, and delays repolarization [8]. These effects can produce severe dysrhythmias, including sinus bradycardia that may progress to fatal ventricular fibrillation [9]. Although neriifolin is a cardiac toxin that can penetrate the CNS, it also exhibits potent anticancer activity against prostate cancer by inducing apoptosis through the CHOP-C/EBP pathway of ER stress, while causing DNA damage and double-strand breaks [10]. Peruvoside, despite its strong cardiotoxicity, can inhibit cancer cell growth by downregulating Cyclin D1 and c-Myc, inducing cell-cycle arrest at the G₀/G₁ or G₂/M phases, and activating caspase-mediated apoptosis. It also shows strong antiviral activity [11,12]. Thevetoxin exhibits similar toxicological effects and acts through comparable pathways, including mechanisms implicated in anticancer activity [13,14].

CT leaves contain a wide range of phytochemicals, several of which are also present in the milky sap. Leaf extracts contain cardenolides (cardiac glycosides), iridoid glucosides, and pentacyclic triterpenes. Fresh leaf extracts also contain neolupenyl acetate, lupeol acetate, oleanolic acid, ursolic acid, stigmast-5-en-7-one, β-sitosterol, kaempferol, quercetin and their glycosides, apiosyl glucoside, and several monoterpenoids [15]. Bark extracts contain neriifolin, thevefolin, peruvoside, and theviridoside, while root extracts contain several pyranosyl derivatives of theviridoside [16]. The fruit pericarp and flowers are rich in flavonoids, including quercetin, eugenol, kaempferol, hesperetin-7-glucoside, and epiperuviol acetate, and also contain β-amyrin. Seed kernels contain substantial amounts of cardioactive glycosides, mainly thevetin A and B [17]. The seeds are also rich in neriifolin, thevetin A and B, thevefolin, theveneriin, and peruvoside, along with fatty oils, flavonoids, and a few phenolic compounds [18]. The fatty oils contain oleic, palmitic, stearic, linoleic, and arachidic acids. In addition, the oil contains a few steroids and triterpenoids, such as α- and β-amyrins, and flavonoids like apigenin and quercetin [19]. Tannins and saponins are abundant in seeds and leaf extracts, providing defensive action. The nitrogenous components identified in the plant are mainly nucleobases, amino acids, and their metabolites, including nicotinic acid [20]. The coumarins and phenolic derivatives serve as allelopathic and antimicrobial agents, inhibiting pathogens. Therefore, the extracts also act potently against major human pathogens like Staphylococcus aureus, Escherichia coli, or Candida albicans owing to their extreme cytotoxicity [21]. CT’s severe toxicity is mainly caused by its cardiac glycosides, or cardenolides, particularly thevetin A and B, peruvoside, and neriifolin. These compounds disrupt the heart’s electrical and mechanical functions by interfering with cellular ion exchange [22]. Their effects depend on three key structural components: the steroid nucleus, the lactone ring, and the sugar moiety. The tetracyclic C₂₃ steroid core helps the molecule bind within myocardial cell membranes, while the unsaturated five-membered γ-lactone ring at C17 forms critical hydrogen bonds with Na⁺/K⁺-ATPase. The sugar groups attached at C3 determine the compound’s lipid or water solubility and influence its absorption. After entering the bloodstream, cardenolides bind to the extracellular domain of Na⁺/K⁺-ATPase on cell membranes. The lactone and steroid portions bind tightly to the α-subunit in its phosphorylated E2-P state, disabling the pump and blocking the normal export of three Na+ ions and the import of two K⁺ ions. As sodium accumulates in the cytoplasm, the reduced sodium gradient weakens the Na⁺/Ca²⁺ exchanger. Ca⁺² then builds up in the sarcoplasmic reticulum and cytoplasm, causing serious electrical and mechanical dysfunction in myocardial cells, including delayed afterdepolarizations, arrhythmias, severe bradycardia, and potentially fatal ventricular fibrillation. Elevated extracellular potassium is an important clinical marker of CT poisoning [22]. In general terms, CT toxicity is sometimes described by the claim that ingesting one seed is comparable to taking 100 digoxin tablets, making exposure potentially fatal. Recommended treatment includes anti-digoxin Fab antibody and fructose 1,6-diphosphate, together with cardiovascular supportive care [23].

Below are several important phytochemicals identified in the entire plant.

Analysis of the dried seeds has shown several isoquinoline and Amaryllidaceae-type alkaloids, which are hordenine, lycorine, galanthamine, crinine, ismine, trisphaeridine, anhydrolycorine, assoanine, galanthine, incartine, and galwesine. However, they exist in trace amounts and are not responsible for the severe poisoning [Adhikari D, Ghosh T, Ghosh R. J Stress Physiol Biochem, 2023, 19(4), 178 – 202.]

Traditional medicinal role: CT has a wide range of ethnobotanical uses, most commonly as a cardiotonic, laxative, or topical remedy; however, every part of the plant is highly toxic and may be fatal to humans and animals [7]. In some regions, traditional practitioners use highly diluted extracts or the plant’s milky sap for heart-related conditions such as cardiac weakness or edema [7]. CT extracts have also been used historically in ointments for skin disorders, including rashes and infections, and occasionally for joint discomfort [24]. Bark and leaf extracts are used to treat fever, malarial fever, severe constipation, and intestinal worms, and may also be given as emetics or febrifuges [7]. Seed extracts have been used as abortifacients and for skin complaints, hemorrhoids, inflammation, and rheumatism, and are sometimes claimed to have anticancer effects. Plant extracts have also shown several beneficial activities, including antioxidant, immunomodulatory, antiparasitic, antifungal, and antimicrobial effects [25].

Pharmacological effect: The pharmacological effects of CT are overshadowed by its highly active cardiac glycosides, even though the plant contains a large reserve of other bioactive secondary metabolites exhibiting numerous diverse effects. Despite extreme toxicity, CT plays a few beneficial pharmacological roles for health.

Anti-inflammatory effect – Although CT is unsafe for human use, laboratory studies indicate that extracts from its leaves, flowers, and seeds may reduce pain and inflammation. Their effects resemble those of non-steroidal anti-inflammatory drugs (NSAIDs), acting both peripherally and centrally by suppressing pro-inflammatory mediators [24]. Because antioxidant activity is closely linked to inflammation control, CT’s anti-inflammatory mechanism appears to depend largely on scavenging reactive oxygen species (ROS), thereby limiting enzyme-driven production of inflammatory mediators. This activity is mainly attributed to its abundant flavonoids and terpenoids, along with some cardiac glycosides [7,26].

Antioxidant activity – In vitro studies show that CT extracts have significant antioxidant activity, as measured by DPPH and FRAP assays, by donating electrons that stabilize reactive oxygen species (ROS) and neutralize free radicals [27]. The main active constituents include phenolics and flavonoids, such as quercetin and kaempferol, as well as several tannins and terpenes [28]. By neutralizing singlet and triplet oxygen, these compounds help inhibit oxidative lipid degradation in cell membranes, supporting CT’s strong antioxidant potential.

Anticancer effect – Numerous in vitro studies suggest that CT bioactive compounds have strong cytotoxic and antiproliferative effects against several human cancer cell lines. However, in vivo studies have not been conducted because the plant is extremely cardiotoxic in humans, largely due to its abundant cardiac glycosides. These compounds strongly inhibit the Na⁺/K⁺-ATPase pump, disrupting ionic balance and cellular energy processes, triggering self-destruction, and arresting the cell cycle at the G₂/M phase; both in vitro and in vivo animal studies support these effects [29]. Together, these biochemical events lead to apoptosis. Methanolic seed extracts appear to be the most potent. The cancer cell lines tested have primarily included breast (MCF-7), prostate (PC3), lung (A549), and colon (HCT-116), with IC₅₀ values generally ranging from 39 to 110 µg/ml. Notably, no cytotoxicity has been observed in non-tumorigenic or normal cell lines. The extracts also reduce tumor-cell motility and adhesion, which may help limit metastasis by preventing spread to other tissues or organs. Flavonoids and phenolics, particularly thevetiaflavone, may further contribute through antioxidant activity [30].

Antidiabetic effect – Leaf and bark extracts of CT have shown strong glucose-lowering activity in laboratory studies using both in vitro and in vivo models. In streptozotocin-induced diabetic rats, methanolic bark extract at 200 mg/kg body weight significantly reduced blood glucose levels, with effects comparable to metformin at 10 mg/kg [31]. The extracts also improved abnormal lipid profiles by lowering total cholesterol, triglycerides, and LDL while increasing HDL [31]. These effects may be mediated by ROS-scavenging flavonoids, phenolics, tannins, saponins, and related compounds, which act as antioxidants and inhibit enzymes such as α-glucosidase and α-amylase, thereby slowing carbohydrate absorption [32]. Despite these promising antihyperglycemic effects in diabetic rat models, ingestion of any CT extract or plant part should be avoided because of its severe toxicity.

Antispermatogenic effect – Animal studies indicate that CT may reduce sperm production and male fertility. The active compounds implicated include α-amyrin acetate, lupeol acetate, α-amyrin, β-amyrin, lupeol, and thevetigenin. Oral administration of methanolic stem-bark extract at 100 mg/rat/day for two weeks significantly reduced reproductive organ weights and sialic acid levels in the epididymides, testes, seminal vesicles, and ventral prostate. It also decreased spermatogenic elements and markedly reduced the nuclear diameter of Leydig cells, seminiferous tubules, and Sertoli cells. Sperm density and motility were substantially reduced, suggesting inhibition of spermatogenesis and a possible contraceptive effect [33]. This effect may hinder sperm penetration through cervical mucus and lower the likelihood of fertilization. Biochemical analyses showed significantly reduced testicular 17β-hydroxysteroid dehydrogenase (17β-HSD) and Δ5,3β-hydroxysteroid dehydrogenase (Δ5,3β-HSD) activities after extract treatment. Treated animals also had lower SOD and peroxidase activities, increased lipid peroxidation, and histological damage to germ cells in the seminiferous tubules. Overall, CT’s antispermatogenic activity may involve suppressed testosterone and gonadotropin levels, oxidative free-radical generation, and germ-cell damage that disrupts spermatogenesis without causing evident metabolic toxicity [34].

Gastroprotective effect – Laboratory studies suggest that CT has gastroprotective, antiulcer, and antinociceptive activities by protecting the gastric lining from chemical irritants and reducing tissue inflammation [35]. These effects have been observed after oral administration or inhalation of CT volatile oil, whose major identified constituents are linalool and 1,8-cineole. The oil strongly reduces acetic acid-induced writhing in a naloxone-sensitive manner. Its analgesic effect after inhalation is blocked by pretreatment with naloxone and atropine, suggesting involvement of opioidergic and cholinergic pathways. In the experimental model, linalool plus 1,8-cineole alone did not produce a significant response, indicating that other constituents, such as flavonoids and terpenoids, may also contribute. For gastric protection, oral CT oil, linalool, or 1,8-cineole protected against ethanol-induced ulcers but not indomethacin-induced ulcers, suggesting that the effect does not involve the arachidonic acid metabolic pathway [35,36].

Anthelmintic effect – CT shows notable in vitro anthelmintic activity, inducing paralysis and death in parasitic worms. Laboratory studies have used Indian earthworms because their anatomy resembles that of human intestinal roundworms, enabling comparative efficacy testing. Methanolic leaf extract at 20–100 mg/ml paralyzed earthworms within 8–10 minutes and killed them within 11–22 minutes. Under similar conditions, albendazole API, a commercial drug, acted more slowly, requiring 24–45 minutes to induce paralysis and 38–65 minutes to cause death. The bioactive fraction contains tannins, saponins, alkaloids, and flavonoids [37].

Antimicrobial effect – CT exhibits significant antimicrobial activity against a broad range of pathogenic bacteria and fungi, largely because of its diverse phytochemical content. In vitro studies show that flower, leaf, and seed extracts can inhibit microbial growth by disrupting cell-membrane integrity, ultimately leading to cell death [38]. The main active constituents include tannins, phenols, and alkaloids. Phenols and tannins interfere with key microbial enzymes, while flavonoids damage cell membranes and, after entering the cell, inhibit nucleic acid synthesis. Alkaloids also exert bactericidal effects by altering membrane permeability [38]. Reported activity includes Gram-positive bacteria such as Staphylococcus aureus, Bacillus cereus, and Enterococcus faecalis; Gram-negative bacteria such as Escherichia coli, Pseudomonas aeruginosa, and Salmonella typhi; and fungi such as Candida albicans, Rhizopus, and Curvularia lunata. Its efficacy is comparable to that of the standard antibiotic chloramphenicol. Methanol, ethanol, and chloroform extracts appear to be more active than aqueous extracts [39,40].

Antidiarrheal effect – Animal studies show that ethanolic CT leaf extract has significant antidiarrheal activity, reducing intestinal motility and fluid accumulation and possibly acting against bacterial pathogens. In albino rats, it inhibited castor oil-induced diarrhea. The extract appears effective at low doses, but higher doses may be lethal. Its activity is mainly attributed to flavonoids and tannins, which relax intestinal smooth muscle, slow intestinal transit, and allow the colon to reabsorb water more efficiently [41].

Toxicity: All parts of CT are highly toxic to humans and animals because they contain cardiac glycosides that can fatally disrupt normal heart function. Although these cardenolides are potentially lethal, some are used cautiously for selected cardiac conditions, similar to digoxin [22]. In addition, several CT-derived compounds have shown potential anticancer activity and may have future value in cancer therapy [30].

Bibliography

1. “Cascabela thevetia – Plant Finder” –  www.missouribotanicalgarden.org
2. Langford S D, Boor P J. Toxicology, 1996, 109(1), Bibcode:1996 Tox.109. https://doi.org/10.1016%2F0300-483X%2895%2903296-R
3. https://www.smgrowers.com/products/plants/plantdisplay.asp?plant_id=1737
4. https://apps.cals.arizona.edu/arboretum/taxon.aspx?id=275
5. https://horticultureunlimited.com/cascabela-thevetia-yellow-oleander-lucky-nut/
6. Sarwade P P, Maurya C, Pant N C et al. J Res Appl Sci Biotechnol, 2024, 3(5), 211 – 221. https://doi.org/10.55544/jrasb.3.5.22
7. Bhagya N. Natl Prod Res, 2025, 1- 16,  https://doi.org/10.1080/14786419.2025.2572039
8. https://www.ebmconsult.com/articles/mechanism-of-action-digoxin-inotropy-force-contraction-heart
9. Nyegaard M, Overgaard M T, Sondergaard M T et al. Amer J Human Genet, 2012, 91(4), 703 – 712. https://doi.org/10.1016/j.ajhg.2012.08.015
10. Zhao W, Li G, Zhang Q et al. Biochem Pharmacol 2023, 209, 115453. https://doi.org/10.1016/j.bcp.2023.115453
11. Lai Y, Chang H, Chen H et al. Amer J Cancer Res. 2022, 12(6), 2576 – 2593.
12. Wu K X, Yogarajh T, Loe M W C et al. Acta Pharm Sin B, 2023, 13(5), 2039 – 2055. https://doi.org/10.1016/j.apsb.2023.03.015
13. Eriyawa A, Jayamanne S, Lokunaragoda N et al. PloS One, 2025, 20(3), e0320301.  https://doi.org/10.1371/journal.pone.0320301
14. Sristy S, Singh G. Int J Creative Open Res Eng Mange, 2026, 02(05), 1 – 13. https://doi.org/10.55041/ijcope.v2i5.759
15. Essiett U, Udolfa I. Scum Eur J Biomed Pharm Sci, 2014, 1, 35 – 44.
16. Bawaazeer S. Int J Appl Pharmceut, 2021, 13(Spl Issue 1), 79 – 82.
17. Shriyan A, More V, Purandare S et al. The Ind J Pediat, 2011, 78, 364 – 365.
18. Eddleston M, warrell D. 1999, “Management of acute yellow oleander poisoning”, Vol-92, pp. 483 – 485. Oxford University Press.
19. Mishra U, Singh A, Singh S. Int J Sci Res Technol, 2026, 3(8), 143 – 155.
20. Mekky R H, Hamed M Z, Temraz A et al. Chem Biodiver, 2026, 23, e01869. https://doi.org/10.1002/cbdv.202501869
21. Zaynab M, Khan J, Al-Yahyai R et al. Toxicon, 2024, 250, 108118. doi: 10.1016/j.toxicon.2024.108118
22. Lamichhane S, Lamichhane G, Naharki K et al. Discover Plants, 2026, 3(68), https://doi.org/10.1007/s44372-026-00548-6
23. Shivraja A, Shruti A, Sudha Reddy V R. Int J Contempo Pediatr, 2018, 5(4), 1690 – 1692. doi.org/10.18203/2349-3291.ijcp20182591
24. Rahman N, Rahman H, Haris M, Mahmood R.  J Trad Complement Med, 2017, 7(4), 519 – 525. https://doi.org/10.1016/j.jtcme.2017.01.005
25. Mishra U, Singh A, Singh S K. Int J Sci R Tech, 2026, 3(8), 143 – 156.
26. Chamakuri S R, Priyanak D, Hussain S A et al. Plant Arch, 2021, 21(2), 290 – 294.
27. Muralidharan K, Paul P, Pushpa V et al. Int J Bot Stud, 2024, 9(12), 16 – 19.
28. Seetharaman S, Indra V, Sunder N, Geetha S. J Pharmacogn Phytochem, 2017, 6(3), 93 – 97.
29. Rajhans S, Pandya H, Kumar S P et al. J Nat Remed, 2023, 23(1), 89 – 104. https://doi.org/10.18311/jnr/2023/30525
30. Ramos-Silva A, Tavares-Carreon F, Figueroa M et al. BMC Compli Altern Med, 2017, 17, 241. DOI 10.1186/s12906-017-1727-y
31. Gogol N, Bhuyan B. Int J Pharm Pharmaceut Sci, 2017, 9(6), 48 – 53.
32. Sukhikh S, Babich O, Prosekov A et al Metabolites, 2023, 13(4), 513. https://doi.org/10.3390/metabo13040513
33. Gupta R, Kachhawa J B S, Gupta R S et al. Human Fertility, 2011, 14(1), 53 – 59. https://doi.org/10.3109/14647273.2010.542230
34. Mondal P, Bera P R, Maitry R et al. Int J Pharma Sci Res, 2024, 15(1), 177 – 186.
35. Kumar P, Shukla P. Adv Med Plant Res, 2015, 3(3), 113 – 119.
36. Cherrada N, Chemsa A E, Gheraissa N et al. Food Sci Nutr, 2024, 12(11), 8793 – 8824. https://doi.org/10.1002/fsn3.4536
37. Prusty B, Hotta S K. World J Pharma Pharmaceut Sci, 2023, 12(9), 1626 – 1636. https://doi.org/10.20959/wjpps20239-25631
38. Adhikari D, Ghosh T, Ghosh R. J Stress Physiol Biochem, 2023, 19(4), 178 – 202.
39. Khan A N, Aldowairy N N A, Alorfi H S S et al. Processes, 2022, 10, 1949. https://doi.org/10.3390/pr10101949
40. Selvaraj S. Indra V, Sundar N, Geetha S. J Pharmacogn Phytochem, 2017, 6(3), 93 – 97.
41. Hassan M M, Saha A K, Khan S A et al. Open Vet J, 2011, 1, 28 – 31.