The therapeutic effect and mechanism of Chinese medicine Xuan-Yun-Ding on posterior circulation ischemia with vertigo in a rabbit model.

The aim of research is to unveil the mechanisms of the beneficial effects of XYD on PCIV in a rabbit model. 40 New Zealand white rabbits were randomly divided into 5 groups,including normal control group (NC), model control group (MC), low-dose of XYD group (LXYD), high-dose of XYD group (HXYD) and Yang-Xue-Qin-Nao group (YXQN). PCIV rabbit model was established by feeding high-fat diet companied with paravertebral sclerotherapy and rotation exercise. The general observation, step-down test, rheoencephalogram, blood tests, histopathological detection and the plasma concentration of the effective component of XYD were investigated. After pharmacological intervening, the step-down time, REG, PL, IPL, blood viscosity, the levels of blood lipids, CRGP were significantly improved. Moreover, the vertebral artery showed the reduced stenosis of arterial lumen and less proliferation of fibrous tissue in the arterial wall in the LXYD, HXYD and YXQN group. Based on the LC-MS detection, the blood concentrations of puerarin in the LXYD and HXYD group were significantly increased after pharmacological intervening. XYD could ameliorate the symptoms of vertigo, Qi-deficiency and blood stasis in PCIV rabbits via effectively regulating the levels of blood lipids and vasoactive substances, decreasing blood viscosity, increasing CBF and protecting vestibular function.

Autophagy is involved in regulating VEGF during high-glucose-induced podocyte injury.

Podocytes are the major sites of vascular endothelial growth factor (VEGF) production in kidneys. Over-expression of VEGF is involved in the pathogenesis of diabetic nephropathy (DN), and an emerging body of evidence suggests that autophagy plays an important role in DN. In this study, the effect of autophagy on over-expressed VEGF along with its underlying mechanism was investigated in streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-induced podocytes. We found that diabetes caused podocyte foot process effacement and VEGF upregulation significantly. In vitro, high glucose induced VEGF and reduced the podocyte viability. After treatment with rapamycin in podocytes, an autophagy inducer, VEGF activation was significantly abrogated and podocyte injury was ameliorated. In contrast, podocytes treated with 3-methyladenine (3-MA), a potent autophagy inhibitor, had increased VEGF expression. Furthermore, 3-MA significantly increased the production of HG-induced reactive oxygen species (ROS), whereas rapamycin decreased the cellular ROS level. Inhibition of ROS production by N-acetyl-l-cysteine (NAC) effectively reduced the over-expression of VEGF. These studies show the vital role of autophagy in the regulation of VEGF, which presents a protective effect on HG-induced podocyte injury. ROS production may be an important mechanism for mediating this process.