Antihepatotoxic effect of Nymphaea stellata willd., against carbon tetrachloride-induced hepatic damage in albino rats
Introduction
The liver regulates many important metabolic functions. Hepatic injury is associated with distortion of these metabolic functions (Wolf, 1999). Thus, liver diseases remain one of the serious health problems. Inspite of tremendous strides in the modern medicine, there are not much drugs available for the treatment of liver disorders (Chaterrjee, 2000a). Nymphaea stellata willd. (Nymphaceae), a medicinal plant has been mentioned for the treatment of liver disorders in Ayurveda, an ancient system of medicine (Nadakarni, 1954). But this plant has not been subjected to systematic investigation to assess its hepatoprotective effect. To the best of our knowledge, only one report dealing with the preliminary investigation to asses its hepatoprotective effects is available (Chaterrjee, 2000b).
Keeping this fact in view, the present study was undertaken to investigate the hepatoprotective activity of Nymphaea stellata willd., flower against carbon tetrachloride-induced hepatic damage in albino rats.
Section snippets
Plant material and extraction
Nymphaea stellata willd., flowers were locally collected in the month of March, washed, dried and powdered in grinding mill. Dr. Mrs. Alka Chaturvedi from Department of Botany, Nagpur University, Nagpur, India authenticated the plant, where a voucher specimen of the plant was deposited (Acc. No. 5773/A). The 10% extract was then prepared in 20% alcohol. This was then kept for 14 days with daily shaking and then filtrate was used for treatment (the extract when concentrated the yield was found
Results and discussion
It is well established from the earlier studies that the cleavage of carbonchloride bond (CCl bond) of carbon tetrachloride leads to the formation of trichloromethyl peroxy radical (CCl3·O2−), which is involved in the pathogenesis of liver injury (Cheeseman et al., 1985, Slater, 1978).
The abnormal higher level of serum ALT, AST, ALP and bilirubin observed in our study (Table 1) is the consequence of carbon tetrachloride-induced liver dysfunction and denotes the damage to the hepatic cells (
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