Effect of GABA on oxidative stress in the skeletal muscles and plasma free amino acids in mice fed high-fat diet.

Increased levels of plasma free amino acids (pFAAs) can disturb the blood glucose levels in patients with obesity, diabetes mellitus and metabolic syndrome (MS) and are associated with enhanced protein oxidation. Oxidation of proteins, especially in the muscles, can promote protein degradation and elevate the levels of pFAAs. Gamma-aminobutyric acid (GABA), a food additive, can reduce high-fat diet (HFD)-induced hyperglycaemia; however, the mechanisms remain unclear. The aim of this study was to evaluate the effects of GABA on protein oxidation and pFAAs changes. One hundred male C57BL/6 mice were randomly divided into five groups that were fed with control diet, HFD and HFD supplied with 0.2%, 0.12% and 0.06% GABA in drinking water for 20 weeks respectively. HFD feeding led to muscular oxidative stress, protein oxidation, pFAA disorders, hyperglycaemia and augmented plasma GABA levels. Treatment with GABA restored normally fasting blood glucose level and dose-dependently inhibited body weight gains, muscular oxidation and protein degradation. While medium and low doses of GABA mitigated HFD-induced pFAA disorders, the high dose of GABA deteriorated the pFAA disorders. Medium dose of GABA increased the levels of GABA, but high dose of GABA reduced the levels of plasma GABA and increased the activity of succinic semialdehyde dehydrogenase in the liver. Therefore, treatment with GABA mitigated HFD-induced hyperglycaemia probably by repairing HFD-induced muscular oxidative stress and pFAA disorders in mice. Our data also suggest that an optimal dose of GABA is crucial for the prevention of excess GABA-related decrease in the levels of pFAA and GABA as well as obesity.

[The effects of jiexinkang on the apoptosis of leukemic cells].

UNLABELLED: The effects of Chinese medicine jiexinkang(JXK) on apoptosis of leukemic cells were studied by morphology approach and electrophoresis of DNA fragments. RESULTS: 1. The apoptotic cells and apoptotic bodies were found by electrical microscopy and the typical ladders of DNA fragments were detected by electrophoresis. 2. JXK induced apoptosis of leukemic cells(HL-60 and K562) in a certain range of concentration and at appropriate time. The time to K562 cell apoptosis was longer than that of HL-60 and its dosage was larger than that of HL-60. CONCLUSION: HL-60 and K562 leukemic cell apoptosis may be induced by JXK and there is correlation between dose and time. The study provides experimental evidences for the clinical treatment of leukemia.