Objective: The motor thalamus plays an important role during exercise. It aims to observe the changes of mGluR4 and mGluR5 in ventrolateral thalamus of rats induced by repeated exhaustive exercise, and to discuss the relationship of mGluR4, mGluR5 and oxidative damage occured during exhaustive exercise. Methods: There were 48 male wistar rats, which were randomly divided into four groups including CG, 0EG, 24EG and 48 EG, each group having 12 rats. Meanwhile, immunohistochemistry (IMM) technique was used to investigate the expression of positive cell and integrated optical density (IOD) of metabotropic glutamate receptor 4 (mGluR4) and metabotropic glutamate receptor 5 (mGluR5), and the impact of exhaustive exercise played on oxidative stress indexes such as malondialdehyde (MDA), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) in ventrolateral thalamus of rats were also investigated in different groups. Results: Compared with CG, the expression of mGluR4 and mGluR5 protein of ventrolateral thalamus in 0EG and 24EG both significantly increased, and the value of mGluR4 in 48EG were still higher than control group, however the the value of mGluR5 in 48EG reduced to the rest level of control group. Meanwhile, the SOD activities of 0EG and 24EG group were significantly higher than the control group, and it was the same with GSH content in ventrolateral thalamus of rats. Meanwhile, MDA has been investigated that it increased significantly in 0EG and 24EG compared with control group, and the MDA level of 48EG was still significant higher than CG. Moreover, the indexes of muscle injury such as LD, CK and BUN all increased significantly post-exercise immediately and post-exercise 24 hours .Conclusion: Exercise fatigue could result in up-regulation of mGluR4 and mGluR5 and increace activity of SOD , GSH-PX and MDA in ventrolateral thalamus of rats, and it also induce the muscle injury by increase the level of LD, CK and BUN in serum, which suggested that ventrolateral thalamus was an important brain rigion to modulate the motor function, and mGluR4 and mGluR5 maybe two important receptors prevent from the increase of free radicals and muscle injury induced by exercise fatigue.
Objectives: The gastrointestinal side effects of mycophenolic acid affect its efficacy in kidney transplant patients, which may be due to its toxicity to the intestinal epithelial mechanical barrier, including intestinal epithelial cell apoptosis and destruction of tight junctions. The toxicity mechanism of mycophenolic acid is related to oxidative stress-mediated the activation of mitogen-activated protein kinases (MAP K). Schisandrin A (Sch A), one of the main active components of the Schisandra chinensis, can protects intestinal epithelial cells from deoxynivalenol-induced cytotoxicity and oxidative damage by antioxidant effects. The aim of this study was to investigate the protective effect and potential mechanism of Sch A on mycophenolic acid-induced damage in intestinal epithelial cell. Methods: Caco-2 cells monolayers were treated with mycophenolic acid (10µM) and/or Sch A (10, 20 and 40µM) at 37°C for 24h, and cell viability was measured by MTT; Western blot and immunofluorescence were used to detect the expression of relevant proteins. Intracellular ROS and apoptosis were measured by flow cytometry, and malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by kits. Results: The results showed that Sch A significantly reversed the mycophenolic acid-induced cell viability reduction, restored the expression of tight junction protein ZO-1, occludin and reduced cell apoptosis. In addition, Sch A inhibited mycophenolic acid-mediated MAPK activation and reactive oxygen species (ROS) increase. Conclusions: Sch A protected intestinal epithelial cells from mycophenolic acid intestinal toxicity, at least in part, by reducing oxidative stress and inhibiting MAPK signaling pathway. Conclusions: Sch A protected intestinal epithelial cells from mycophenolic acid intestinal toxicity, at least in part, by reducing oxidative stress and inhibiting MAPK signaling pathway.
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