Methanol Extract of Chasmanthera dependens Stem Mitigates against Mechanisms Involved in Piroxicam-induced Liver Damage in Rat

Chasmanthera dependens has been claimed by tradition healers as a therapeutic agent in many diseases including hepatotoxicity. This study sought to evaluate the possible mechanisms involved in the hepatoprotective potential of tannin-rich extract of Chasmanthera dependens stem (TRECDS).

Thirty two male Wistar rats (100- 130 g) were divided into four groups of eight rats per group labelled as group 1,2,3 and 4. The rats were treated orally for ten days consecutively. Group 1 served as control group and received normal saline, group 2 rats received 40 mg/kg piroxicam alone, groups 3-4 were treated with 40 mg/kg piroxicam and 200 and 400 mg/kg TREDS respectively concomitantly. All the experimental rats were fed with standard rat chows. Twenty four hours after, blood was collected to obtain serum; liver was excised to prepare homogenate and histology staining under pentobarbital sodium anaesthesia. Liver function test (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT)) and oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO)) biomarkers were assessed. Pro-inflammatory cytokines (tumor necrosis factor-α (TNF- α), interleukin-1β (IL-1β)) and apoptotic markers; caspase-3 (CASP-3) and caspase-9 (CAPS-9), cytochrome-c (CYT-c)) were also assessed.

The results showed that piroxicam administration caused hepatic damage as was evident in the histological assessment with increased serum activities of liver function markers, levels of pro-inflammatory cytokines and apoptotic markers. TRECDS also showed significant attenuation of the oxidative stress by decreasing the LPO level and increasing the activities of SOD, CAT and GSH level.

Oral administration of TRECDS also restores the morphological structure of the liver in a dose-dependent manner.

Conclusion: Oral administration of TRECDS exhibited protective potential against piroxicam-induced hepatotoxicity.