Objective: To investigate the effect of peroxide reductase 1 (Prdx1) on myocardial hypertrophy and fibrosis in spontaneously hypertensive rats，and to analyze its mechanism． Methods: Forty five SHR rats were randomly divided into model group (SHR group) ，AAV9-NC group and AAV9-Prdx1 group．There were 15 WKY rats in each group，and the other 15 Wistar Kyoto rats were set as the control group．The rats in each group were administered continuously for 8 weeks，and the indexes of cardiac function were detected by echocardiography ; The mean blood pressure and myocardial hypertrophy were measured ; HE staining and Masson staining were used to observe the histomorphology and fibrosis of rat myocardium ; The indexes of oxidative stress in rat serum were detected by ELISA ; The expression level of Prdx1 mRNA in rat myocardium was detected by qRT-PCR ; Western blot was used to detect the expression of Prdx1 protein and nuclear factor E2 related factor 2 (Nrf2) / heme oxygenase-1 (HO-1) signaling pathway related proteins in rat myocardium. Results: Compared with the Control group，the expression of Prdx1 mRNA and protein ，left ventricular ejection fraction ( EF) and left ventricular shortening rate ( FS) decreased in SHR group (P＜0. 05) ，the mean blood pressure，heart mass index ( HMI) and left ventricular mass index (LVMI) of rats increased (P＜0. 05) ，and there were obvious pathological damage and collagen fiber deposition in myocardial tissue．The activities of superoxide dismutase (SOD) and glutathione peroxidase ( GSH-Px) in rat serum decreased，and the content of malondialdehyde (MDA) increased (P＜0. 05) ; The expression of Nrf2， HO-1 and quinone oxidoreductase 1 (NQO1) protein decreased in myocardial tissue (P＜0. 05) ．Compared with SHR group，the expression of Prdx1 mRNA and protein，EF and FS in myocardial tissue of AAV9-Prdx1 group increased (P＜0. 05) ，the mean blood pressure，HMI and LVMI of rats decreased (P＜0. 05) ，and myocardial tissue injury and myocardial fibrosis improved ; The activities of SOD and GSH-Px in rat serum increased，while the content of MDA decreased (P＜0. 05) ; The expression of Nrf2，HO-1 and NQO1 protein increased in myocardial tissue (P＜0. 05) ． Conclusion Overexpression of Prdx1 can reduce myocardial hypertrophy and fibrosis and improve cardiac function in SHR rats．Its mechanism may be related to activating Nrf2 / HO-1 signaling pathway and inhibiting oxidative stress response.

Objective To investigate the neuroprotective effect of methylene blue on diabetic retinopathy in rats. Methods Thirty SD rats were randomly divided into blank, control and experimental groups. The control and experimental groups were induced with diabetes by streptozotocin (STZ) intraperitoneal injection. After 6 weeks of successful modeling, the experimental group received intravitreal injection of methylene blue at a dose of [0.2 mg/(kg.d)], while the control group received an equal amount of dimethyl sulfoxide (DMSO) intravitreal injection, both continuously injected for 7 days. ELISA was used to detect the levels of retinal superoxide dismutase (SOD), 8-iso-prostaglandin F2alpha (iPF2α) and interleukin-1β (IL-1β) in rats. Western blot analysis was used to detect the expression of retinal extracellular signal-regulated kinase 1/2 phosphorylation (p-ERK1/2) and phosphorylated protein kinase B (p-AKT), and PAS staining was used to detect retinal morphological changes. Results Compared with the blank group rats, the retinal SOD activity in the control and experimental group rats was significantly reduced. iPF2α, IL-1β and p-ERK1/2 level increased, while p-AKT level decreased. Compared with the control group, the SOD activity of the experimental group rats increased. iPF2α and IL-1β level went down, while p-ERK1/2 and p-AKT level went up significantly. The overall thickness of the retinal layer and the number of retinal ganglion cells were significantly reduced. Conclusion Methylene blue improves diabetic retinopathy in rats by reducing retinal oxidative stress and enhancing ERK1/2 and AKT phosphorylation.
Rats ; Animals ; Diabetic Retinopathy/metabolism* ; Proto-Oncogene Proteins c-akt/metabolism* ; Mitogen-Activated Protein Kinase 3/metabolism* ; Interleukin-1beta/metabolism* ; Methylene Blue/pharmacology* ; Phosphorylation ; Rats, Sprague-Dawley ; MAP Kinase Signaling System ; Diabetes Mellitus, Experimental/drug therapy* ; Superoxide Dismutase/metabolism*