Abstract
In the previous studies, it was revealed that Mitragyna rotundifolia Kuntze (MR) had strong antioxidant activity in vitro. Oxidative stress is considered to play a prominent causative role in the development of various hepatic disorders. n-Butanol extract from M. rotundifolia barks (MRBBU) and leaves (MRLBU) were investigated, and it played a protective role against carbon tetrachloride (CCl4)-induced acute liver injury in mice. The degree of protection has been measured by using biochemical parameters, such as serum glutamic pyruvic transaminase (GPT), serum glutamic oxaloacetic transaminase (GOT), malondialdehyde (MDA) and superoxide dismutase (SOD) in liver tissue homogenate. The results of the intragastric administration of MRBBU (300, 150 and 75 mg/kg body weight per day, respectively) and MRLBU (300, 150 and 75 mg/kg body weight per day, respectively) on CCL4-induced acute liver injury in mice for 8 days demonstrated that the level of GPT and GOT in each treatment group decreased significantly (P < 0.001). It was observed that the level of liver MDA in MRLBU (75 mg/kg) group did not significantly decreased (P > 0.05), but that in the other treatment groups significantly decreased (P < 0.01 and P < 0.05, respectively). With the exception of MRLBU group (150 and 75 mg/kg) (P > 0.05), the level of SOD in other treatment groups significantly increased (P < 0.001, P < 0.01 and P < 0.05, respectively). Results indicated that MR has hepatoprotective effect against CCl4-induced oxidative damage in mice, and the hepatoprotective effect may be correlated with its antioxidant effects. Key words: Mitragyna rotundifolia Kuntze, antioxidant activity, carbon tetrachloride, hepatoprotective effect.
Highlights
Liver injury can be induced by various factors, and hepatotoxins, such as CCl4, ethanol and acetaminophen which are metabolized by cytochrome P450 2E1 (CYP2E1) (Sun et al, 2001)
Oxidative stress is considered to play a prominent causative role in the development of various hepatic disorders. n-Butanol extract from M. rotundifolia barks (MRBBU) and leaves (MRLBU) were investigated, and it played a protective role against carbon tetrachloride (CCl4)-induced acute liver injury in mice
The results of the intragastric administration of MRBBU (300, 150 and 75 mg/kg body weight per day, respectively) and MRLBU (300, 150 and 75 mg/kg body weight per day, respectively) on CCL4-induced acute liver injury in mice for 8 days demonstrated that the level of glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) in each treatment group decreased significantly (P < 0.001)
Summary
Liver injury can be induced by various factors, and hepatotoxins, such as CCl4, ethanol and acetaminophen which are metabolized by cytochrome P450 2E1 (CYP2E1) (Sun et al, 2001). CCl4, the classic heaptotoxin, is widely used to induce liver damage in animal models and to investigate the role of lipid peroxidation as a mediator of hepatic injury (Brattin et al, 1985). The mechanism of CCl4-induced acute liver injury is accepted widely that CCl4 was metabolized to a highly reactive trichloromethyl radical (CCl3-) by cytochrome P450 in liver. CCl3- in liver can induce lipid peroxidation and leads to hepatocellular membrane damage (Ohta et al, 1998; Drill, 1952). The defensive provided by antioxidant systems is crucial in liver injury and disease
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
