PMCCPMCCPMCC

Search tips
Search criteria 

Advanced


 
Formats
Article sections
Authors
Related links
Logo of ayuHomeCurrent issueInstructionsSubmit article
 
Ayu. 2012 Jan-Mar; 33(1): 119–122.
PMCID: PMC3456849
Copyright : © AYU (An International Quarterly Journal of Research in Ayurveda)
Anticonvulsant activity of raw and classically processed Vacha (Acorus calamus Linn.) rhizomes
Savitha D. Bhat, B. K. Ashok,1 R. N. Acharya,2 and B. Ravishankar3
Lecturer, Department of Dravyaguna, Muniyal Institute of Ayurveda Medical Sciences, Manipal, Karnataka, India
1Research Assistant, Pharmacology laboratory, Department of Dravyaguna, Institute for Post Graduate Teaching and Research in Ayurveda, Gujarat Ayurved University, Jamnagar, Gujarat, India
2Associate Professor, Department of Dravyaguna, Institute for Post Graduate Teaching and Research in Ayurveda, Gujarat Ayurved University, Jamnagar, Gujarat, India
3Director, SDM Research Centre for Ayurveda and Allied Sciences, Kuthpady, Udupi, Karnataka, India
Address for correspondence: Dr. Savitha D. Bhat, Lecturer, Department of Dravyaguna, Muniyal Institute of Ayurveda Medical Sciences, Manipal, Karnataka, India. E-mail: anudivas/at/yahoo.co.in
This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
The rhizome of Vacha (Acorus calamus) has been used in Ayurvedic medicine for the treatment of various ailments, such as epilepsy, headache, eye disorders, insomnia, loss of memory, etc. Previous studies demonstrated that Vacha rhizome is having significant anticonvulsant activity against various induced seizures models in experimental animals. Ayurvedic pharmacopoeia of India has advocated Shodhana (purificatory procedures) to be done prior to its use. In the present study a comparative anticonvulsant activity of raw and Shodhita (classically processed) Vacha rhizomes were screened against Maximal Electro Shock (MES) seizure model to assess the effect of classical purificatory procedure on pharmacological action of Vacha. Phenytoin was used as standard antiepileptic drug for comparison. Pretreatment with both raw and classically processed Vacha samples exhibited significant anticonvulsant activity by decreasing the duration of tonic extensor phase. Further classically processed Vacha statistically decreased the duration of convulsion and stupor phases of MES-induced seizures. The results obtained from the present study clearly confirmed the anticonvulsant activity of raw Vacha and subjecting to classical Shodhana procedure did not alter the efficacy of Vacha rhizomes instead it enhanced the activity profile of the Vacha.
Keywords: Acorus calamus, anticonvulsant, epilepsy, phenytoin, shodhana, vacha
Acorus calamus Linn. (Family: Acoraceae) is a semi-evergreen perennial medicinal plant with scented rhizomes, arching tapered reed-like leaves and minute yellow-green flowers. It is known as Vacha in Ayurveda and the rhizome of this plant has been used since ancient times for its beneficial role as brain tonic (Medhya).[1] It has also been reported to possess tranquilizing,[2–5] antimicrobial,[6] antidiarrheal,[7] antidyslipidemic,[8] neuroprotective,[9] antioxidant,[10] anticholinesterase,[11,12] spasmolytic,[13] antiulcer,[14] anthelmintic,[15] anti-inflammatory, and analgesic[16,17] activities. Most of these functions are attributed to the aromatic oil present in the rhizome.[18],[19] Further the essential oil from Acorus has been reported to be having antiepileptic activity against seizures induced by various means.[20–24]
Ayurvedic classics have emphasized various methods of Shodhana (purificatory procedures) to overcome the undesired effects from various poisonous and nonpoisonous drugs.[25,26] Even though Vacha does not come under poisonous drug category, some Ayurvedic texts and Ayurvedic pharmacopoeia of India have recommended Shodhana for Vacha rhizome.[27,28] The reason behind this Shodhana procedure though clearly not mentioned by any of the texts, it may be presumed to reduce the Tiksnata and emetic actions of rhizome. Till date not a single work has been reported on activity profile of classically processed Vacha, hence in this study Vacha rhizomes were subjected to classical purificatory procedure and a comparative anticonvulsant activity evaluation of raw and classically processed rhizomes were undertaken as a preliminary study to evaluate the role of classical purificatory procedure in modifying the therapeutic efficacy.
Plant materials
Rhizomes of A. calamus were collected from its natural habitat in the forest regions of Yelagiri hills, Tamilnadu in the month of November in fully matured condition.[29] The plant material was identified and authenticated by the Pharmacognosist of IPGT & RA, Gujarat Ayurved University, Jamnagar. The roots and old leaf scars were removed, washed thoroughly in water to remove the soil adhered to it, and then dried in partial shade. The rhizomes were cut uniformly into smaller pieces and divided into two parts. The first part was coded as sample raw Vacha (RV) and the second part was utilized for Shodhana. The Shodhana procedure involved boiling of Vacha samples successively by Gomutra, Mundi kwatha (decoction prepared from whole plant of Sphaeranthus indicus Linn.), Panchapallava kwatha (decoction prepared from a group of five leaves), and Gandhodaka (decoction prepared from a group of aromatic herbs) as described in Ayurvedic text.[27] After Shodhana procedure the rhizomes were shade dried for 12 days and marked as sample Shodhita Vacha (SV). Then both RV and SV were powdered (Mesh 80) and utilized for screening of anticonvulsant activity.
Animals
Charles–Foster strain albino rats weighing 200 ± 10 g were obtained from animal house (Registration No.548/2002/CPCSEA) attached to Pharmacology laboratory. Six animals were housed in each cage made up of polypropylene with stainless steel top grill. The dry wheat (posthulled) waste was used as bedding material and was changed every morning. The animals were acclimatized for 7 days before commencement of the experiment in standard laboratory conditions 12 ± 01 hour day and night rhythm, maintained at 25 ± 3°C and 50%–70% humidity as per Committee for the Purpose of Control and Supervision of Experimental Animals (CPCSEA) guidelines. Animals were provided with balanced food (Amrut brand rat pellet feed supplied by Pranav Agro Mills Pvt. Limited) and water ad libitum. Protocol used in this study for the use of animals was approved by the institutional animal ethics committee (Approval number: IAEC 06/09-11/PhD/08). The animals were fasted overnight before the experiment.
Dose selection and schedule
The dose of Vacha as per Ayurvedic Pharmacopoiea of India is 120 mg per day.[28] The dose for experimental animals was calculated by extrapolating the human dose to animals based on the body surface area ratio by referring to the standard table of Paget and Barnes.[30] On this basis the rat dose of Vacha samples (RV and SV) was found to be 10.80 mg/kg rat and is rounded to 11 mg/kg. The test drug was suspended in distilled water with suitable concentration depending on the body weight of animals and administered orally with the help of gastric catheter sleeved to syringe. Phenytoin sodium was selected as standard antiepileptic drug (RS) and administered in the dose of 25 mg/kg (i.p).[31]
Anticonvulsant activity against maximal electroshock seizures
The rats were pretested 24 h prior to administration of test drugs for sensitivity to electric shock and those failing to give hind limb tonic extension were rejected. Thus screened animals were divided in to four groups of six animals each. Group 1 served as control, received equivalent amount of the vehicle (distilled water). Group 2 and 3 received RV and SV samples of Vacha, respectively. Fourth group received phenytoin sodium as standard antiepileptic drug. Experiment was conducted at the same time each day and 60 min after vehicle/drug administration (Phenytoin was given 30 min before the application of electroshock). Seizures are induced to all the groups by using an Electro-convulsiometer and elicited by a 60 Hz alternating current of 150 mA intensity for 0.2s. A drop of electrolyte solution (0.9% NaCl) with lignocaine was applied to the corneal electrodes prior to application to the rats. The duration of various phases of epilepsy were recorded.[32]
Statistical analysis
The data were expressed as mean ± standard error mean (SEM). The significance of differences among the groups was assessed using one-way analysis of variance and the test followed by Dunnett's test. P values less than 0.05 were considered as significant.
Pretreatment with RV and SV exhibited significant anticonvulsant activity by decreasing the duration of tonic extensor phase [Table 1]. Further RV-treated group showed 31.76% protection, while SV showed 36.48% protection against MES induced seizures. Both the samples of Vacha shortened other phases of MES-induced seizures, such as flexion, convulsion, and stupor, however, only the observed decrease of clonus and stupor in SV-treated group was found to be statistically significant. The standard drug phenytoin had exhibited significant anticonvulsant effect by abolishing the tonic extension phase. Further it significantly shortened all other phases induced by MES.
Table 1
Table 1
Effect on MES-induced seizures in rats
Maximal Electro-Shock seizure is one of the commonly used models for preliminary testing of anticonvulsant drugs that produces generalized tonic–clonic seizures. This test serves to identify compounds that prevent seizure spread, corresponding to generalized tonic–clonic seizures in humans.[33] It has often been stated that antiepileptic drugs that block MES-induced tonic extension act by blocking seizure spread, moreover MES-induced tonic extension can be prevented either by drugs that inhibit voltage dependent Na+ channels or by drugs that block glutaminergic excitation mediated by the N-methyl-d-aspartate (NMDA) receptor.[34] Phenytoin is effective in therapy of generalized tonic-clonic and partial seizures have been found to show strong anticonvulsant action by increasing brain content of Gamma-Amino Butyric Acid (GABA) in MES test.[35,36] In the present study treatment with RV and SV significantly inhibited the MES-induced seizures. Because inhibition of the MES test predicts activity against generalized tonic–clonic and cortical focal seizures, activity against MES-induced seizures suggests that both RV and SV samples are useful in suppressing generalized tonic–clonic seizures by regulating GABA-mediated synaptic inhibition. Koo et al. and Liao et al. showed that pre-inhalation of the essential oil of acorus markedly delayed the appearance of pentylenetetrazole-induced convulsion by inhibiting the activity of gamma-amino butyric acid (GABA) transaminase.[23,24] The same mechanism may be involved in observed activity profile. Furthermore, pretreatment with SV significantly decreased the duration of convulsion and stupor phases of MES-induced seizures. This shows that SV sample is having a better anticonvulsant activity. This may be attributed to acquiring of some active principles from shodhana dravya, such as gomutra (cow urine) and Mundi Kwatha (decoction of S. indicus Linn.), which are reported to be having anticonvulsant activity.[37,38]
Conclusion
The results obtained from the present study clearly confirmed the anticonvulsant activity of Vacha. Subjecting to classical Shodhana procedure did not lessen the efficacy of Vacha rhizomes instead it enhanced the activity profile of the Vacha.
Acknowledgments
Authors are thankful to Prof. M.S. Baghel, Director, IPGT and RA, Gujarat Ayurved University, Jamnagar, for the constant support and providing financial support and facilities to carry out this study.
References
1. Pandey GS, editor. Bhavaprakasha Nighantu. India: Chaukhambha Bharati Academy; 2006. Bhavamishra; p. 44.
2. Danilevskii NF, Antonishin BV. Antimicrobial activity of a tincture of Japanese pagoda tree (Sophora japonica) and of the essential oil of sweet flag (Acorus calamus) Mikrobiol Zh. 1982;44:80–2. [PubMed]
3. Maj J, Malec D, Lastowski Z. Pharmacological properties of native Calamus (Acorus calamus) I., effect on essential oil on the central nervous system. Dissertations Pharm. 1964;16:447–56.
4. Agarwal SL, Dandiya PC, Sing KP, Arora RB. A note on the preliminary studies of certain pharmacological actions of Acorus calamus. J Am Pharm Assoc. 1956;45:655–6. [PubMed]
5. Menon MK, Dandiya PC. The mechanism of tranquillizing action of asarone from Acorus Calamus Linn. J Pharm Pharmacol. 1967;19:170–5. [PubMed]
6. Zaiba IA, Beg AZ, Mahmood Z. Antimicrobial potency of selected medicinal plants with special interest in activity against phytopathogenic fungi. Indian Vet Med J. 1999;23:299–306.
7. Shoba FG, Thomas M. Study of antidiarrhoeal activity of four medicinal plants in castor-oil induced diarrhoea. J Ethnopharmacol. 2001;76:73–6. [PubMed]
8. Parab RS, Mengi SA. Hypolipidemic activity of Acorus calamus L. in rats. Fitoterapia. 2002;73:451–5. [PubMed]
9. Shukla PK, Khanna VK, Ali MM. Protective effect of Acorus calamus against acrylamide induced neurotoxicity. Phytother Res. 2002;16:256–60. [PubMed]
10. Acuna UM, Atha DE, Ma J. Antioxidant capacities of ten edible North American plants. Phytother Res. 2002;16:63–5. [PubMed]
11. Oh MH, Houghton PJ, Whang WK. Screening of Korean herbal medicines used to improve cognitive function for anti-cholinesterase activity. Phytomedicine. 2004;11:544–8. [PubMed]
12. Mukherjee PK, Kumar V, Mal M, Houghton PJ. Invitro Acetylcholinesterase inhibitory Activity of the Essential Oil from Acorus Calamus and its main constituents. Planta Medica. 2007;73:283–5. [PubMed]
13. Gilani AH, Shah AJ, Manzoor A. Antispasmodic effect of Acorus calamus Linn. is mediated through calcium channel blockade. Phytother Res. 2006;20:1080–4. [PubMed]
14. Rafatullah S, Tariq M, Mossa JS, Al-Yahya MA, Al-Said MS, Ageel AM. Anti-secretagogue, anti-ulcer and cytoprotective properties of Acorus calamus in rats. Fitoterapia. 1994;65:19–23.
15. Raj KR. Screening of some indigenous plants for anthelmintic action against Ascaris lumbricoides. Indian J Physiol Pharmacol. 1974;18:129–31. [PubMed]
16. Derle DV, Gujar KN. Anti-inflammatory, analgesic and antipyretic activity of Acorus calamus and Curcuma amada. Indian Drugs. 2001;38:444.
17. Varde BA, Ainapure SS, Naik SR, Amladi SR. Anti-inflammatory activity of coconut oil extract of Acorus calamus, Ocimum sanctum and Ocimum basilicum in rats. Indian Drugs. 1988;25:226–8.
18. Gupta AK, Tandon N. Reviews on Indian Medicinal Plants. Vol. 1. New Delhi, India: Indian Council of Medical Research; 2004. p. 200.
19. Mittal N, Ginwal HS, Varshney VK. Pharmaceutical and biotechnological potential of Acorus calamus Linn.: An indigenous highly valued medicinal plant species. Phcog Rev. 2009;3:93–103.
20. Madan BR, Arora RB, Kapila K. Anticonvulsant, antiveratrinic, and antiarrhythmic actions of Acorus calamus, an Indian indigenous drug. Arch Int Pharmacodyn Ther. 1960;124:201–11. [PubMed]
21. Cho J, Kong JY, Jeong DY, Lee KD, Lee DU, Kang BS. NMDA receptor-mediated neuroprotection by essential oils from the rhizomes of Acorus gramineus. Life Sci. 2001;68:1567–73. [PubMed]
22. Yang L, Li S, Wang Y, Huang Y. Effects of Acorus gramineus and its main component alpha-asarone on the reactivity and convulsive threshold of immature rats to electric stimulation. Neural Regen Res. 2006;1:78–80.
23. Koo BS, Park KS, Ha JH, Park JH, Lim JC, Lee DU. Inhibitory effects of the fragrance inhalation of essential oil from Acorus gramineus on central nervous system. Biol Pharm Bull. 2003;26:978–82. [PubMed]
24. Liao WP, Chen L, Yi YH, Sun WW, Gao MM, Su T, et al. Study of antiepileptic effect of extracts from Acorus tatarinowii Schott. Epilepsia. 2005;46:21–4. [PubMed]
25. Shastri Brahmashankar. Yogaratnakara. Varanasi: Chaukamba Amarabharati Prakashan; 2007. p. 169.
26. Acharya Yadavji Trikamji. Rasamrutam. In: Joshi Damodar., editor. Rasayogavijnaneeyam. Varanasi: Chaukamba Amarabharati Prakashan; 2003. p. 284.
27. Dwivedi Ramanath., editor. Chakradatta. Varanasi: Chaukamba Sanskrit Samsthan; 2005. Chakrapanidatta; p. 155.
28. 1st ed. Part II. Vol. 1. New Delhi: Ministry of health and family welfare, Govt of India; 2007. Anonymous. The Ayurvedic pharmacopoeia of India; pp. 245–7.
29. Rajanighantu Narahari, Pandit, Tripathi I, Varga D. Varanasi: Chowkhamba Krishnadas Academy; 2003. p. 26.
30. Paget GE, Barnes JM. Evaluation of drug activities. In: Lawrence DR, Bacharach AL, editors. Pharmacometrics. Vol. 1. New York: Academic Press; 1964. p. 161.
31. Senthil Kumar KK, Rajkapoor B. Effect of Oxalis corniculata extracts on biogenic amines concentrations in rat brain after induction of seizure. Int J Phytopharmacol. 2010;1:87–91.
32. Goodman LS, Grewal MS, Brown WC, Swinyard EA. Comparison of maximal seizures evoked by pentylenetetrazol (Metrol) and electroshock in mice, and their modification by anticonvulsants. J Pharmacol Exp Ther. 1953;108:168–76. [PubMed]
33. Kupferberg HJ. Antiepileptic drug development program: A cooperative effort of government and industry. Epilepsia. 1989;30:51–6. [PubMed]
34. Ragwaski MA, Porter RJ. Antiepileptic drugs and pharmacological mechanisms and clinical efficacy with consideration of promising development stage compounds. Pharmacol Rev. 1995;42:223–86. [PubMed]
35. White HS. Clinical significance of animal seizure models and mechanism of action studies of potential antiepileptic drugs. Epilepsia. 1997;38:9. [PubMed]
36. McDonald RL, Kelly KM. Antiepileptic drugs: Mechanism of action. Epilespsia. 1991;34:51–8.
37. Achliya SG, Wadodkar GS, Dorle AK. Evaluation of sedative and anticonvulsant activities of Unmadnashak Ghrita. J Ethanopharmacol. 2004;94:77–83. [PubMed]
38. Nanda BK, Jena J, Rath B, Behera B. Anticonvulsant Activity of whole parts of Sphaeranthus indicus Linn. extract in Experimental Mice. Drug Invent Today. 2010;2:202–6.
Articles from Ayu are provided here courtesy of
Medknow Publications