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Aim To evaluate the protective effect of Averrhoa Carambola L. Roots DMDD alleviating myocardial injury in diabetes mellitus (DM) mice and its mechanism. Methods SD mice were given high-glucose-high-fat diet combined with streptozotocin to induce DM model, and were administered with DMDD. The fasting blood glucose (FBG) was recorded. The left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), maximum upstroke velocity of left ventricular pressure (+ dp/dt
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Aim To investigate the neuroprotective effect and mechanism of salidroside (Sal) on rats with permanent middle cerebral artery occlusion model (pMCAO) by regulating the PI3 K/AKT signaling pathway. Methods A total of 80 healthy adult SPF male SD rats were randomly divided into sham operation group (sham group), model group (pMCAO group), drug administration group (pMCAO + Sal group) and inhibitor group (pMCAO + Sal + YL group). After the pMCAO model rats were prepared by the line bolt method, salidroside (50 mg · kg
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Aim To explore the effect of chrysin on chondrocyte autophagy in rat chondrocyte osteoarthritis model induced by lipopolysaccharide and its mechanism. Methods Normal articular cartilage cells of 10 SPF SD rats were isolated and cultured in vitro, and the autophagy of rat chondrocytes was induced by LPS. The experiment was divided into blank control group, LPS group, chrysin (CHR) group and LPS + CHR group, the activity of cells in each group was detected by CCK-8 method, the mitochondrial membrane potential of cells in each group was detected by Rhodaminel23, and the protein expression of PI3K, AKT, p-PI3K, p-AKT, Beclin-1 and LC3 II in cells of each group was detected by reactive oxygen species, Western blot method of DCFH-DA. Results Chrysin could inhibit the autophagy induced by LPS, especially when the concentration of chrysin was 10 mmol · L
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Aim To explore whether propofol attenuates neuroinflammation and brain damage via modulating PI3K/Akt signaling pathway following focal cerebral ischemia in rats, and further investigate the possible mechanisms. Methods Sprague-Dawley rats which underwent the cerebral ischemic injury by the suture occlusion model were randomly divided into sham operation, MCAO, propofol-treated and LY294002 groups. Neurological deficit scores, cerebral infarct size, and cerebral water content were measured , then the myeloperoxidase (MPO) activities in rat brain were measured as an index of neutrophil infiltration. The content of TNF-α and IL-1β in blood was determined using ELISA; the expressions of p-Akt and Akt in rat brain were detected by Western blot. Results Propofol reduced neurological deficit scores, cerebral infarct size, cerebral water content, MPO activity , TNF-α and IL-1β content, which were all abolished by LY294002. Propofol up-regulated the expression of p-Akt, which was inhibited by LY294002. Conclusion Propofol attenuates neuroinflammation and ischemic brain damage via modulating the PI3K/Akt signaling pathway.
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The resistance to PBK-Akt-mTOR pathway inhibitors has close relationship to the negative feedback of its context-dependent signal pathways. According to our current understanding, the resistant mechanisms could be divided into the following basic conditions: related to FOXO and hormone receptor, MYC-dependence, β-catenin-dependence, JAK/STAT pathway-dependence, MAPK pathway-dependence and related to AXL. The emergence of drug resistance to PBK-Akt-mTOR pathway inhibitors has greatly limited their curative effect. The reported resistance mechanisms to PBK-Akt-mTOR pathway inhibitors to search for potential strategies for overcoming resistance by drug combination were summarized.