Anti-BAX monoclonal antibody

Diabetic cardiomyopathy (DCM) is a major diabetes-related microvascular disease. LncRNA MALAT1 is widely expressed in cardiomyocytes responding to hypoxia and high levels of glucose (high glucose). In this study, cardiac fibroblasts (CFs) were transfected with si-MALAT1 and exposed to high glucose. CFs in the high glucose groups were treated with 30 mmol/L glucose, and the control CFs were treated with 5.5 mmol/L glucose. The expression of MALAT1 in the nucleus and cytoplasm of CFs was detected. The biological behavior of CFs, as well as collagen production, activity of the Hippo-YAP pathway, and nuclear localization of YAP were measured. Mouse models of DCM were established to observe the pathological changes to myocardium and determine the levels of collagen I, Bax, and Bcl-2. The interaction between MALAT1 and YAP was analyzed, and CREB expression in the high-glucose treated CFs was detected. MALAT1 was upregulated in high-glucose CFs and located in the nucleus. High-glucose increased collagen production, inflammation, cell proliferation, cell invasiveness, and phosphorylation of MST1 and LATS1, and also promoted nuclear translocation of YAP. These trends in high-glucose treated CFs and the DCM mice were reversed by transfection with si-MALAT1. MALAT1 positively regulated the nuclear translocation of YAP by binding to CREB. CREB levels were increased in the high-glucose CFs, but decreased after silencing MALAT1. These results indicate that si-MALAT1 reduces inflammation and collagen accumulation in high-glucose CFs and DCM mice via the Hippo-YAP pathway and CREB.

Flavonoids have been reported to have therapeutic potential for spinal cord injury. Hawthorn leaves have abundant content and species of total flavonoids, and studies of the effects of the total flavonoids of hawthorn leaves on spinal cord injury have not been published in or outside China. Therefore, Sprague-Dawley rats were used to establish a spinal cord injury model by Allen's method. Rats were intraperitoneally injected with 0.2 mL of different concentrations of total flavonoids of hawthorn leaves (5, 10, and 20 mg/kg) after spinal cord injury. Injections were administered once every 6 hours, three times a day, for 14 days. After treatment with various concentrations of total flavonoids of hawthorn leaves, the Basso, Beattie, and Bresnahan scores and histological staining indicated decreases in the lesion cavity and number of apoptotic cells of the injured spinal cord tissue; the morphological arrangement of the myelin sheath and nerve cells tended to be regular; and the Nissl bodies in neurons increased. The Basso, Beattie, and Bresnahan scores of treated spinal cord injury rats were increased. Western blot assays showed that the expression levels of pro-apoptotic Bax and cleaved caspase-3 were decreased, but the expression level of the anti-apoptotic Bcl-2 protein was increased. The improvement of the above physiological indicators showed a dose-dependent relationship with the concentration of total flavonoids of hawthorn leaves. The above findings confirm that total flavonoids of hawthorn leaves can reduce apoptosis and exert neuroprotective effects to promote the recovery of the motor function of rats with spinal cord injury.