Ethnobotanical Leaflets 13: 910-16. 2009.
Hepatoprotective Effect of Cassia Fistula Linn.
*S.J. Wasu and B.P. Muley
Siddhivinayak College of Pharmacy, Warora, Chandrapur- 442 907, India
A number of herbal preparations are used throughout the world for the management of the hepatic disorders. However, many of them have not been investigated for their described effects. Cassia fistula Linn. is one such drug used in the treatment of hepatitis in folk medicine. Therefore, an attempt was made to investigate the hepatoprotective effect of leaves and bark of Cassia fistula against carbon tetrachloride (CCl4) induced hepatotoxicity in rats. Sixty albino Wistar rats were divided into six equal groups of 10. Four groups received extracts leaves/bark of Cassia fistula and intraperitoneal (i.p.) CCl4 (0.2 ml/100 g) either before or after administration of extracts. Two groups were controls, one treated with CCl4 and one with normal saline. Liver damage was assessed by plasma concentration of bilirubin and enzyme activities of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase. Treatment with aqueous extract of leaves and bark significantly reduced CCl4 -induced elevation in plasma enzyme and bilirubin concentration in rats. This study demonstrated that CCl4 -induced liver damage in rats can be ameliorated by treatment of extracts from leaves and bark.
KEYWORDS: Cassia fistula, hepatoprotective effect, aminotransferases, carbon tetrachloride.
Liver is the key organ for detoxification and disposition of endogenous substances. It is continuously and widely exposed to xenobiotics, hepatotoxins, and chemotherapeutic agents that lead to impairment of its functions1. Cassia fistula (Leguminoceae) is known as amaltas (Hindi), bahava (Marathi). It is a deciduous, medium sized tree upto 24 m in height with straight bole upto 15 m, found both wild and cultivated almost throughout India. The leaves reported to contain flavonoids like quercetin, kaempferol along with anthraquinone glycosides while bark is rich in flavonoids like lupeol, epicatechin and tannins2. Literature survey revealed that no scientific study is reported regarding its hepatoprotective activity of Cassia fistula. Therefore, the present study was conducted to investigate its hepatoprotective activity.
MATERIAL & METHODS
Leaves and bark of Cassia fistula were obtained from Amaravati District, Maharashtra. The plant samples were identified and authenticated in the Herbarium by botanist Dr. Prabha Y. Bhogaonkar, VMV, Botany Department, Amaravati, Maharashtra, India. The leaves and bark were macerated by using water as a menstrum. The obtained extract was dried and concentrated under freezed drier and kept tied closed into container.
Sixty animals were randomly divided equally into six groups of 10 each.
Blood was collected in heparinized tubes from the inner canthus on the 29th day or the 16th day in the pre or post-treated groups, respectively. Plasma was separated by centrifugation at 900 rpm for 10 min at 4°C and used for determining the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and bilirubin concentration using the Hitachi autoanalyzer-902.
Values reported are means ± SE (n = 10). Experimental results were statistically analyzed using the Student's t -test followed by ANOVA. P value less than 0.01 considered significant.
The CCl4 -treated animals exhibited a significant increase (P < 0.01) in plasma enzyme activity and bilirubin concentration compared with saline-treated control rats (Table 1).
Table 1: Effect of pre- and post- treatment with aqueous Cassia fistula leaves and bark on CCl4 induced liver damaged in albino Wistar rats.
CF: Cassia fistula; Data are expressed as ± SE (n=10), * Significantly different than control at P<0.01.
A significant reduction was found in elevated AST, ALT, and ALP values in rats subjected to both pre- and post-treatments with the aqueous extracts of both leaves and bark. Liver enzyme values were higher in the four experimental groups than in the saline-treated controls, but the liver enzyme values were decreased to about half of those found in CCl4 -treated control animals for all liver function tests except bilirubin. Expressed in percentage of protection provided, both Cassia fistula leaves and bark given pre- or post-treatment were hepatoprotective (Table 2).
Table 2: Hepatoprotective activity of leaves and bark of Cassia fistula in CCl4 induced hepatotoxicity in albino Wistar rats.
CF: Cassia fistula; % Protection = 1-(PC-S)/ (C-S) × 100, where PC, C and S are the measurable variables in rats treated with CF leaves or bark extract with CCl4, CCl4 and saline treated animals respectively
Liver cirrhosis induced by CCl4 is perhaps the best-studied model of liver cirrhosis4 .Several mechanisms underlying this toxicity have been suggested5. The reduction of CCl4 -induced elevated plasma activities of AST, ALT, ALP, and bilirubin level in animals pre- and post-treated with the aqueous extracts of Cassia fistula leaves and bark showed their ability to restore the normal functional status of the poisoned liver and also to protect against subsequent CCl4 hepatotoxicity. The mechanism by which the fruits pulp and seeds induces its hepatoprotective activity is not certain. The inactive metabolite (CCl4), is transformed to a free radical through the microsomal cytochrome P-450-dependent enzyme, resulting in activation of CCl4 toxicity. Hepatoprotective activity of any drug is the ability of its constituents to inhibit the aromatase activity of cytochrome P-450, thereby favoring liver regeneration. On that basis, it is suggested that flavonoids in Cassia fistula could be a factor for exhibiting the hepatoprotective activity.
This study clearly demonstrates that aqueous extracts of Cassia fistula leaves and bark are effective in the treatment and prevention of CCl4 -induced hepatic cytotoxicity. The data suggest that the daily oral consumption of an aqueous extract of the Cassia fistula leaves and bark may alleviate CCl4 toxicity and provide protection to liver. This research work supports its traditional use for the treatment of hepatic disorder.
1. Preussmann R 1978. Hepatocarcinogens as potential risk for human liver cancer. In: Remmer H, Bolt HM, Bannasch P (eds). Primary liver tumors. Lancaster: MTP Press; pp. 11-29.
2. Ramchandran K (ed.) 1992. The Wealth of India, A Dictionary of Indian Raw Materials and Industrial Products, Vol-3, Ca-Ci. CSIR, New Delhi.
3. Singh B, Saxena AK, Chandan BK 1998. Hepatoprotective activity of verbenalin on experimental liver damage in rodents. Fitoterapia 69:135-40.
4. Cornelius CE 1993. Animal models in liver research . San Diego: Academic Press; pp. 341.
5. Recknagel RO, Glender EA, Dolak JA, Waller RL 1989. Mechanisms of carbon tetrachloride toxicity. Pharmacol Ther43:139-54.