The present study was designed to investigate the significance of calpain‐1 in the high‐fat diet (HFD)‐induced liver dysfunction and to explore the possible mechanism. C57 mice and calpain‐1 knockout (KO) mice were fed with standard diet (SD) or HFD, respectively, for 16 weeks. The activities of calpain, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and superoxide dismutase (SOD) in serum and/or liver of mouse were measured. Lipid profiles in the serum and liver were examined. Contents of oxidized low‐density lipoprotein (oxLDL), malondialdehyde (MDA), tumor necrosis factor (TNF‐α), and interleukin‐6 (IL‐6) in serum or/and liver were detected. The results showed that compared with C57 mice fed with SD, HFD‐fed C57 mice showed the increased activities of AST and ALT in the serum, which was decreased in calpain‐1 KO mice fed with HFD. In addition, knockout of calpain‐1 decreased the contents of oxLDL, MDA, TNF‐α, and IL‐6, while increased SOD activity, in serum and/or liver. However, knockout of calpain‐1 had no effects on lipid profiles in both serum and liver. When fed with SD, all these parameters of C57 and calpain‐1 KO mice were comparable except for decreased calpain activity in the liver of calpain‐1 KO mice. The results suggested that knockout of calpain‐1 protects against HFD‐induced liver dysfunction through inhibiting oxidative stress and inflammation.
Ulinastatin (UTI) can support protection for several organs through inhibition of the release of inflammatory factors, absorbing oxygen radicals, and inhibition the progression of fibrosis. However, whether UTI has effect on hyperoxia-induced lung injury is still unclear. In this study, the effects of UTI treatment on newborn rats suffering hyperoxia-induced lung injury were examined. The results demonstrated that UTI treatment significantly attenuated the wet/dry weight ratio, downregulated the levels of tumor necrosis factor-α (TNF-α), inhibited macrophage infiltration, and improved the average weight of rats. The most significant changes were observed in high-dose UTI treatment group. However, UTI had no effect on pulmonary superoxide dismutase (SOD) and malondialdehyde (MDA) levels. Our results suggested that Ulinastatin prevents hyperoxia-induced lung injury on newborn rats by downregulating TNF-α and inhibiting macrophage infiltration.
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