Abstract
Ruellia tuberosa L. (RTL) has been used as a folk medicine for curing diabetes mellitus in East Asia decades. This study investigated the effect of RTL on hepatic detoxification enzyme expression in diabetic rats. Male Wistar rats were fed a high fat diet (HFD) and intraperitoneally injected with streptozotocin (STZ) to induce diabetes. Subsequently, rats received oral administrations of 100 or 400 mg kg−1 body weight RTL extract, in either water (RTLW) or ethanol (RTLE), once a day for 4 weeks. The real-time PCR analyses showed that abnormality of hepatic phase I and II detoxification enzyme expression was observed in diabetic rats. However, both RTLW and RTLE significantly normalized the expression of hepatic phase I detoxification enzymes such as CYP 2E1, and expression of phase II detoxification enzymes such as UGT 1A7 and GST M1 in diabetic rats. Furthermore, we found that fasting serum glucose, hemoglobin A1C (HbA1C) and the area under the curve of oral glucose tolerance test (AUCOGTT) levels were significantly reduced in both RTLW and RTLE treated diabetic rats. Moreover, both RTLW and RTLE significantly increased the activity of hepatic anti-oxidative enzymes such as superoxide dismutase (SOD) in diabetic rats. The present study suggests that RTL may ameliorate abnormal hepatic detoxification function via alleviating hyperglycemia and enhancing hepatic antioxidant capacity in HFD/STZ-induced diabetic rats.
Highlights
Diabetes mellitus (DM) is a metabolic disease caused by an insulin secretion de ciency or insulin dysfunction, which leads to hyperglycemia
3.1 Effect of RTLW and RTLE on phase I enzymes in liver of high fat diet (HFD)/STZ rats
The results from the present study indicated that expression of hepatic CYP 2E1 mRNA was signi cantly elevated in diabetic rats (Fig. 1C; p < 0.05), whereas RTLW, RTLE and pioglitazone hydrochloride (Pio)-treatments reduced hepatic CYP 2E1 expression in diabetic rats and normalized the levels to that of normal rats (Fig. 1C; p < 0.05)
Summary
Diabetes mellitus (DM) is a metabolic disease caused by an insulin secretion de ciency or insulin dysfunction, which leads to hyperglycemia. E-mail: scs@ ntnu.edu.tw; Fax: +886-2-23639635; Tel: +886-2-77341437 phase II.[3,4,5] Phase II enzymes are responsible for conjugation These enzymes conjugate phase I-modi ed xenobiotics with highly polar molecules, which converts them into hydrophilic, inactive compounds that can be excreted into the bile, feces, or urine. High levels of blood sugar may increase oxidative stress in human body and result in the abnormality of detoxi cation function in the liver of DM patients.[6] Impairments in detoxi cation cause accumulations of exogenous or endogenous xenobiotics, which become toxic in the body.[7,8,9] In addition, reactive oxygen species (ROS) are produced during phase I, which can increase the risk of liver injury and reduce the detoxi cation capacity of the liver.[10]
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