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 lens-induced 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.

A novel and simple oral colon-specific drug delivery system based on the pectin/modified nano-carbon sphere nanocomposite gel films.

The 3-aminopropyltriethoxysilane modified nano-carbon sphere (MNCS) was added into pectin-Ca2+ film to improve the controlled release properties of the pectin-based oral colon-specific drug delivery system (OCDDS). The FT-IR measurements indicated the successful modification of nano-carbon sphere via silylation reaction and the electrostatic interaction between the pectin molecules and MNCS in the composite film. The FE-SEM showed the pore structure when the MNCS was mingled with the pectin. The 5-fluorouracil (5-FU) was employed as the drug model and the controlled release properties of the corresponding OCDDSs were determined. The values of the encapsulation efficiency ranged from 30.1% to 52.6%. All composite film based OCDDSs presented higher encapsulation efficiency than single pectin-Ca2+ based OCDDS. The drug release studies emerged that almost all the OCDDSs from composite films presented better release properties than single pectin-Ca2+ based OCDDS. The sample C revealed best release performance with the cumulative release rate of 32.17%, 22.77% and 63.89% in the simulated gastric fluid, small intestinal fluid and colon fluid, respectively. In addition, the kinetics studies were performed to analyze the release data. The cytotoxicity assay indicated good biocompatibility of the composite carriers.