AIM: To explore the effect of syntaxin 17（STX17） on autophagy and amyloid deposition in mouse hippocampal neuronal HT22 cells and its underlying mechanism. METHODS: Lentivirus-mediated overexpression of amyloid precursor protein（APP） and STX17 in HT22 cells was performed, and RT-qPCR was used to detect the relative mRNA expression of APP and microtubule-associated protein 1 light chain 3-II（LC3-II） and STX17 after lentivirus infection. Congo red staining was used to observe amyloid deposition in HT22 cells. The protein expression levels of LC3-II and P62 were detected by Western blot. The localization of STX17 as well as the localization and number of LC3-II puncta were observed by immunofluorescence. RESULTS: After overexpression of APP in HT22 cells, the deposition of amyloid increased, and the expression of STX17 decreased and was mainly located in the cytoplasm（P＜0. 05）. The expression levels of LC3-II and P62 were significantly increased. After lentivirus-mediated overexpression of STX17, the expression levels of LC3-II and P62 were significantly decreased, and the amyloid deposition was also decreased（P＜0. 05）. CONCLUSION: STX17 decreased amyloid deposition in Alzheimer disease by regulating autophagy.

Objective To investigate the role of period 2 (Per2) protein in the death of cardiomyocytes induced by β1-adrenergic receptor autoantibodies (β1-AA). Methods Sixteen male SD rats aged 6~8 weeks were randomly divided into active immunization (model) group and control group (n=8). The model group was immunized with the second extracellular loop of beta1-adrenoceptor (β1-AR-EC Ⅱ), and the control group was injected with Na2CO3 and other solutions. The rat serum was subsequently collected at 8 weeks, followed by the purification of β1-AA. H9c2 cardiomyocyte were selected and randomly divided into control group, β1-AA group, and β1-AR+β1-AA group. Cell viability of each group was detected by CCK-8 assay (n=8). Then H9c2 cells in the control group and β1-AA 1 μmol/L group were synchronized with dexamethasone for 4 h, the expression of Per2 in cardiomyocytes at different circadian time (CT) points was measured by Western blotting, and JTK_CYCLE was used to analyze the circadian rhythm parameters (n=11). Moreover, Per2 in H9c2 cells was knocked down or overexpressed by lentiviral shPer2 and lentiviral Per2, respectively; RT-PCR and Western blotting were performed to detect the changes of Per2 expression (n=6). On the basis of knockdown (n=8) or overexpression (n=10) of Per2, the H9c2 cells were further treated with β1-AA, and the cell survival rate was tested by CCK-8 assay. Results CCK-8 assay showed that the survival rate of H9c2 cells was significantly decreased after β1-AA treatment (P < 0.05). Western blotting demonstrated that β1-AA remarkably inhibited the rhythmic expression of Per2 protein in the cardiomyocytes (JTK_CYCLE, P>0.05), with the decrease at CT8 and CT16 most obviously (P < 0.01). Knockdown of Per2 expression reduced the survival rate of cardiomyocytes, which was further lowered after β1-AA treatment (P < 0.001). However, overexpression of Per2 notably reversed the decline in H9c2 survival rate induced by β1-AA (P < 0.001). Conclusion Per2 protein inhibits β1-AA induced H9c2 cardiomyocyte death.

Objective: To probe the effect of L-carnitine on energy metabolism during renal ischemic reperfusion injury and the possible mechanisms.Methods: Model of renal ischemia-reperfusion was established,and 48 SD healthy rats were divided into untreated control and L-carnitine treated groups.Within each group,rats were further divided into four subgroups,Sham,and 1 h,6 h and 12 h IR group(n =6).The levels of blood serum urea nitrogen(Bun)and creatinine(Scr),the free fatty acid(FFA)content and Na+-K+-ATPase activity in nephritic tissues were measured.The ultrastructural changes in renal tissue were observed under electron microscope.Results: In control groups,compared with those of the sham operation group,Scr and Bun levels at IR6h and IR12h groups increased significantly(P <0.05 or P <0.01);the FFA content in nephritic tissues at IR12h group went up markedly(P <0.01) while the Na+-K+-ATPase activity of IR6h and IR12h groups declined obviously(P <0.05 or P <0.01).As to the L-carnitine treatment groups,compared with those of the control group rats with the same reperfusion time,the Bun levels of 12 h group and the Scr level of IR6h,12h groups were obviously lower(each P <0.01);the FFA content in nephritic tissues at IR12h group was markedly lower while the Na+-K+-ATPase activity was obviously higher(each P <0.01).In addition,ultrastructure indicated injuries of the mitochondriarenal in tubular epithelial cell were attenuated after L-carnitine administration.Conclusion: L-carnitine protects kidney against acute renal ischemia reperfusion injury through promotion of β-oxidation of fatty acids,increasing Na+-K+ ATPase activity,and finally grading-up energy metabolism.