ABSTRACT
PURPOSE: This thesis was to investigate the protective effect and mechanism of H2S-mediated aerobic exercise on the antagonism of the hippocampus inflammatory response in CUMS-depressed mice. METHOD: Seventy C57BL/6 mice were randomly divided into control group (CG), model control group (MG), model exercise group (ME), H2S enhanced group (HG) and H2S enhanced and exercise group (HE). All mice except CG underwent a 28-day CUMS depression model. ME and HE received moderate-intensity aerobic treadmill training for 8 weeks. They were randomly selected for Nissl staining, Immunofluorescence, methylene blue colorimetric assay, and ELISA. The levels of IL-10 and TNF-É were detected by qRT-PCR, and the expression levels of CBS and inflammatory-related factors in the hippocampus were detected. RESULT: Compared with CG, the number of erections, modifications, and crossing grids in MG mice were significantly reduced, the time of forced swimming and forced tail suspension was significantly prolonged, the positive rate of 5-HT decreased, and the symptoms of depression were obvious. The positive rate of CD45+ increased, the inflammatory response was obvious, and the content of H2S and the expression of biosynthetic enzyme CBS decreased. Aerobic exercise and H2S-enhanced mice improved depressive symptoms, decreased proinflammatory factors, increased anti-inflammatory factors, increased H2S content, increased CBS expression, and increased H2S. CONCLUSION: H2S may participate in aerobic exercise to antagonize the inflammatory process of the hippocampus in CUMS-depressed mice by reducing the release of inflammatory response factors and hippocampus nerve injury factors, and effectively alleviate inflammatory injury in the hippocampus of depressed mice.
Subject(s)
Hippocampus , Swimming , Animals , Depression/etiology , Depression/therapy , Mice , Mice, Inbred C57BL , Stress, PsychologicalABSTRACT
Acetaminophen (APAP) overdose can induce liver injury and is the most frequent cause of acute liver failure in the United States. We investigated the role of p62/SQSTM1 (referred to as p62) in APAP-induced liver injury (AILI) in mice. We found that the hepatic protein levels of p62 dramatically increased at 24 h after APAP treatment, which was inversely correlated with the hepatic levels of APAP-adducts. APAP also activated mTOR at 24 h, which is associated with increased cell proliferation. In contrast, p62 knockout (KO) mice showed increased hepatic levels of APAP-adducts detected by a specific antibody using Western blot analysis but decreased mTOR activation and cell proliferation with aggravated liver injury at 24 h after APAP treatment. Surprisingly, p62 KO mice recovered from AILI whereas the wild-type mice still sustained liver injury at 48 h. We found increased number of infiltrated macrophages in p62 KO mice that were accompanied with decreased hepatic von Willebrand factor (VWF) and platelet aggregation, which are associated with increased cell proliferation and improved liver injury at 48 h after APAP treatment. Our data indicate that p62 inhibits the late injury phase of AILI by increasing autophagic selective removal of APAP-adducts and mitochondria but impairs the recovery phase of AILI likely by enhancing hepatic blood coagulation.
ABSTRACT
This study was aimed to investigate the effects of ursolic acid on human hepatic stellate cells (HSC-LX-2) proliferation and its mechanism.Different doses of ursolic acid were incubated with HSC-LX-2 cellin vitrof or 48 h.MTT was used for the detection of HSC-LX-2 cell proliferation.The expressions of PDGF-ERK signaling pathway associated proteins were measured by western blot.The results showed that the proliferation of HSC- LX-2 cells was inhibited by ursolic acid in a dose-dependent manner.The inhibition rate of 20,30 and 40μmol·L-1 of ursolic acid was 9.1%,42.3% and 62.6%,respectively.The IC50 was 35.2μmol·L-1.After incubated with ursolic acid for 48 h,protein levels of PDGF-R and p-ERK in 30 and 40μmol·L-1 group were significantly decreased when compared with the normal group (P<0.05 orP<0.01),except the ERK protein.It was concluded that ursolic acid can inhibit HSC-LX-2 cell proliferation.Its mechanism may be related to the blockage of PDGF-ERK signaling pathway.
ABSTRACT
Objective To establish HPLC method for the determination of naringin in Jizhi droppills. Methods Kromasil C18 (4.6 mm?200 mm, 5 ?m) was used. The mobile phase was consisted of acetonitrile- 1% acetate solution (40∶60). The flow rate was 1.0 mL/min. The UV detection wavelength was at 283 nm. Results The linear range for naringin was 0.07～0.35 ?g, r=0.999 8. The RSD of precision test was 0.3%. The RSD of stability test was 2.3%. The RSD of repeatability test was 1.29%. The average recovery was 98.9%. Conclusion The method of precision and recovery was high, and stability and repeatability was good.
