Electroacupuncture alleviates ciliary muscle cell apoptosis in lens-induced myopic guinea pigs through inhibiting the mitochondrial signaling pathway

AIM:To investigate the effect of electroacupuncture(EA)on the mitochondria-dependent apoptotic signaling pathway in the ciliary muscle of guinea pigs with negative lensinduced myopia(LIM).METHODS:Guinea pigs were randomly divided into normal control(NC)group,LIM group,LIM+SHAM acupoint(LIM+SHAM)group,and LIM+EA group.Animals in the NC group received no intervention,while those in other three groups were covered with-6.0 diopter(D)lenses on right eyes.Meanwhile,animals in the LIM+EA group received EA at Hegu(LI4)combined with Taiyang(EX-HN5)acupoints,while those in the LIM+SHAM group were treated at sham points.After treatments for 1,2,and 4wk,morphological changes in ciliary muscles were observed with hematoxylin and eosin(H&E)staining and nick end labeling(TUNEL),and the expression of the mitochondrial apoptotic signaling pathway-related molecules in ciliary muscles was measured by real-time quantitative polymerase chain reaction(qPCR)and Western blot.Additionally,the adenosine triphosphate(ATP)contents were also determined in ciliary muscles.RESULTS:Axial length increased significantly in the LIM and LIM+SHAM groups and decreased in the LIM+EA group.The ciliary muscle fibers were broken and destroyed in both LIM and LIM+SHAM groups,whereas those in the LIM+EA group improved significantly.TUNEL assay showed the number of apoptotic cells increased in the LIM and LIM+SHAM groups,whereas reduced in the LIM+EA group.ATP contents showed a significant decrease in the LIM and LIM+SHAM groups,whereas increased after EA treatment.Compared with the NC group,the dynamin-related protein 1(DRP1),Caspase3,and apoptotic protease activator 1(APAF1)levels were significantly increased in the LIM group and decreased in the LIM+EA group.CONCLUSION:The results provide evidence of EA inhibiting the development of myopia by regulating the mitochondrial apoptotic signaling pathway.

IL-17 Induces MPTP Opening through ERK2 and P53 Signaling Pathway in Human Platelets

The opening of mitochondrial permeability transition pore（MPTP） plays a critical role in platelet activation. However,the potential trigger of the MPTP opening in platelet activation remains unknown. Inflammation is the crucial trigger of platelet activation. In this study,we aimed to explore whether and how the important inflammatory cytokine IL-17 is associated with MPTP opening in platelets activation by using MPTP inhibitor cyclosporine-A（Cs A）. The mitochondrial membrane potential（Δψm） was detected to reflect MPTP opening levels. And the platelet aggregation,activation,and the primary signaling pathway were also tested. The results showed that the MPTP opening levels were increased and Δψm reduced in platelets administrated with IL-17. Moreover,the levels of aggregation,CD62 P,PAC-1,P53 and the phosphorylation of ERK2 were enhanced along with the MPTP opening in platelets pre-stimulated with IL-17. However,Cs A attenuated these effects triggered by IL-17. It was suggested that IL-17 could induce MPTP opening through ERK2 and P53 signaling pathway in platelet activation and aggregation.