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The Chinese medical mechanism of Huanglian Jieduo Decoction on treating Alzheimer's disease(AD) characterized by "toxin damaging brain collateral" is still unclear. This study aims to explore the mechanism of Huanglian Jieduo Decoction on regulating triggering receptor expressed on myeloid cells 2(TREM2)/protein kinase B(Akt)/glycogen synthase kinase 3β(GSK3β) pathway to improve the cognitive deficit in APP/PS1 transgenic mice. APP/PS1 mice of approximately nine months old were randomly divided into the model group, the low, medium, and high(2.5, 5, and 10 g·kg~(-1)) groups of Huanglian Jiedu Decoction, and 0.75 mg·kg~(-1) donepezil hydrochloride group, and the C57BL/6J mice with the same age were taken as the normal group. After one month of continuous oral administration, a Morris water maze was performed to detect the learning and memory ability of mice. Hematoxylin-eosin(HE) staining was applied to observe the morphology of neuronal cells in the cortical area of mice. Immunofluorescence was used to detect the protein expressions of β-amyloid(Aβ_(1-42)), CD86, and arginase 1(Arg1). The mRNA levels of interleukin(IL)-1β, IL-6, and IL-10 in the cortex of mice were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR). The protein expressions of TREM2, phosphoinositide-3 kinase(PI3K), Akt, GSK3β, and beta-catenin(β-catenin) in mouse cortex were determined by Western blot. The results indicated that the escape latency of the model group was significantly prolonged, and the residence time in the target quadrant and the number of crossing the platform were significantly reduced compared with the normal group. Mice in the model group had a significantly lower number of neurons in the cortex and showed nuclear pyknosis and a significant increase in the expressions of Aβ_(1-42) and CD86. The mRNA levels of IL-1β and IL-6 in tissue were significantly increased, IL-10 were increased, while Arg1 were significantly decreased. The expression of TREM2, p-PI3K(Y607), p-Akt(T308), p-GSK3β(Ser9), and β-catenin in the cortex were significantly down-regulated. Compared with the model group, the escape latency of the mice in the administration group was significantly shortened, and the number of crossing the platform and the residence time in the target quadrant were significantly increased. Furthermore, the number of neurons in the cortex of mice was increased, and nuclear pyknosis was improved. Aβ_(1-42) deposition was decreased significantly. The mRNA levels of IL-1β, IL-6 and CD86 were significantly decreased, while IL-10 and Arg1 levels were significantly increased. The expression of TREM2, p-PI3K(Y607), p-Akt(T308), p-GSK3β(Ser9), and β-catenin protein in the cortex of each administration group was significantly up-regulated compared with the model group. In conclusion, Huanglian Jiedu Decoction reduced the expression of Aβ_(1-42) and neuroinflammation to a neuro-protective effect, thereby improving the learning and memory ability in APP/PS1 mice, which may be related to the TREM2/Akt/GSK3β signaling pathway.

Objective To investigate the protective effect of green tea polyphenol (GTP) on cardiac function in diabetic cardiomyopathy (DCM) rats and its mechanism. Methods After the model of type 1 diabetes was established by streptozotocin induction in rats, they were randomly divided into the following 5 groups for treatment: NG group (n=15), DM group (n=12), GTP group (n=12), GTP+CQ group (n=11), and CQ group (n=12). NG and DM groups were given gastric lavage of distilled water. GTP group was intragastrically administered with GTP [400mg/(kg·d)] solution. CQ group was intragastrically administered with CQ solution [50mg/(kg·d)]. GTP+CQ group was intragastrically administered with CQ and GTP solution of the same volume. Western blot was used to detect the expression of protein related to β-catenin/TCF4/GSK-3β and MTOR pathways in the left ventricular myocardium. Results Compared with those in NG group, the LC3-II/I/ ratio and BECN1 expression were significantly decreased (P<0.05) while SQSTM1 level was significantly increased (P< 0.05) in DM group. The LC3-II/I ratio and BECN1 protein expression level were higher in GTP group than in DM group (P<0.05), while SQSTM1 protein expression level was lower (P<0.05). The protein expressions of β- catenin, TCF4 and MYC were significantly improved in DM group as compared with NG group (P<0.05), and there were higher p-GSK3β/GSK3β and p-MTOR/MTOR ratios in DM group (P <0.05). GTP treatment significantly decreased the protein expressions of β-catenin, TCF4 and MYC, and also decreased p-GSK3β/GSK3β and p-MTOR/ MTOR ratios compared with DM group (P <0.05). Conclusion GTP participates in the protection of heart function in DCM rats by regulating β-catenin/TCF4/GSK-3β and MTOR pathways related to autophagy. [ABSTRACT FROM AUTHOR]

Objective To observe the effect of silencing the expression of ADM using RNA interfering technique on the expression of β-catenin and terminal differentiation of osteosarcoma cells. Methods After the intervention of 0h, 48h and 72h by ADM siRNA, we observed the change of distribution of β-catenin in F5M2 using immunocytochemistry staining. The expression levels of total and phosphorylated β-catenin and GSK3β were detected by Western blot after the intervention by ADM siRNA. The F5M2 cells treated with ADM siRNA were subjected to HE staining, alkaline phosphatase (ALP) assay and immunocytochemistry staining to investigate the biological effects of ADM siRNA on the morphology and terminal differentiation of F5M2 cells. Results After the intervention of 0h, 48h and 72h by ADM siRNA, the distribution of β-catenin was transferred from the cytoplasm to the nucleus. ADM siRNA downregulated the expression level of P-β-catenin and upregulated P-GSK3β detected by Western blot. HE staining revealed that the configuration of F5M2 had undergone restorational changes similar to those of normal cells after ADM siRNA treatment. ALP assay and immunocytochemistry staining showed that the expression of the earlier and later molecular biomarkers of terminal differentiation, including ALP and osteocalcin were strongly positive. Conclusion Silencing the expression of ADM can activate β-catenin to transfer to the nucleus from the cytoplasm, and induce osteosarcoma cells to make terminal differentiation through activating β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

摘 要: 【目的】 研究糖原合成酶激酶3β(GSK3β)抑制在异氟醚后处理减轻SH-SY5Y细胞缺血再灌注损伤的神经保护中所起的作用?【方法】 将SH-SY5Y细胞进行分成3组(n = 24):Control组?OGD组及OGD + Isoflurane组?Control组细胞常规培养;OGD组进行1 h氧糖剥夺(OGD)及20 h模拟再灌注;OGD + Isoflurane组进行1 h的OGD及20 h模拟再灌注,OGD开始时立即暴露于2%异氟醚1 h?检测各组模拟再灌注1 h后LDH释放水平及总GSK3β和磷酸化GSK3β表达水平?将高选择性的GSK3β抑制剂chir 98014 或chir 99021分别加入OGD组或OGD + Isoflurane组,检测各组模拟再灌注1 h后LDH释放水平?【结果】 OGD组LDH释放水平增高,与Control组相比差异有统计学意义(P 0.05),p-GSK3β表达增加,差异有统计学意义(P 0.05)?【结论】 异氟醚后处理对SH-SY5Y细胞缺血再灌注损伤具有神经保护效应?异氟醚后处理保护效应部分通过抑制GSK3β发挥作用?

Objective: To investigate the effect of aerobic exercise on AKT/GSK3β pathway-mediated hepatocyte apoptosis in non-alcoholic fatty liver diseases(NAFLD)., Methods: A total of 30 6-week-old male C57BL/6J mice, and mice were fed adaptively for one week. The control group was fed with ordinary diet, and the model group and model exercise group were fed with high-fat diet until 18 weeks. At the 10th week of the experiment, the model exercise group received aerobic exercise intervention for 8 consecutive weeks until the end of the experiment at the 18th week. Automatic biochemical analyzer to detect serum total cholesterol(TC), triglycerides(TG), alanine aminotransferase(ALT), aspartate aminotransferase(AST), low-density lipoprotein(LDL-C) and high-density lipoprotein(HDL-C) levels. Liver pathological morphology was observed by staining with oil red O and HE. The expression changes of AKT, P-AKT~( Ser473), GSK3β, P-GSK3β~(Ser9) and Caspase-3 proteins were detected by western blot, and the apoptosis of hepatocytes was detected by in situ terminal transferase labeling(TUNEL)., Results: (1) After intervention, compared with control group, body weight, liver index, serum TC, TG, ALT, AST and LDL-C levels in model group were significantly increased(P&lt;0.01 or P&lt;0.05), while HDL-C level was significantly decreased(P&lt;0.01). Compared with model group, body weight, liver index, serum TC, TG, ALT, AST and LDL-C levels in model exercise group were significantly decreased(P&lt;0.01 or P&lt;0.05), while HDL-C level was significantly increased(P&lt;0.01). (2) Compared with the control group, hepatocyte steatosis and the number of lipid droplets in model group were significantly increased. Compared with the model group, the degree of hepatic adipose degeneration was significantly improved and the number of hepatic lipid droplets was significantly decreased in the model exercise group. (3) Compared with control group, the protein expression levels of P-AKT~(Ser473) and P-GSK3β~(Ser9) in model group were significantly decreased(P&lt;0.01 or P&lt;0.05), the protein expression levels of Caspase-3 were significantly increased(P&lt;0.05), and the number of hepatocyte apoptosis was significantly increased(P&lt;0.05). Compared with model group, the expression of P-AKT~(Ser473) and P-GSK3β~(Ser9) protein in model exercise group was significantly increased(P&lt;0.01 or P&lt;0.05), the expression of Caspase-3 protein was significantly decreased(P&lt;0.05), and the number of hepatocyte apoptosis was significantly decreased(P&lt;0.01)., Conclusion: Aerobic exercise can effectively improve NAFLD, by activating AKT/GSK3β pathway and increasing the expression of AKT/GSK3β pathway related molecules, thereby reducing caspase-3 expression and hepatocyte apoptosis.

To observe the effect of puerarin on learning and memory function and tau phosphorylation in APP/PS1 transgenic mice, drugs were administered to 3-month old APP/PS1 transgenic mice. Learning and memory function of mice were assessed by Morris water maze test 3 months after treatment. Animals were decapitated after behavioral test. The levels of Aβ were detected by ELISA, the expression of protein [tau, phosphorylated tau, GSK3β and p-GSK3β(Ser9)] were assessed by Western blot. Morris water maze test showed that the escape latency of APP/PS1 double transgenic mice was significantly longer than that of the normal control group, and the residence time of the original quadrant was significantly shorter. The escape latency of puerarin group was significantly shorter and the residence time of the original quadrant was prolonged compared with the model group. Compared with the normal control group, the levels of Aβ in the cortex of APP/PS1 transgenic mice were increased, the expression of phosphorylated tau was significantly increased, and the expression of phosphorylated GSK3β(Ser9) protein was decreased. Treatment with puerarin, the latency of APP/PS1 transgenic mice was significantly reduced, the level of Aβ was decreased, the expression of phosphorylated tau was significantly decreased, and the expression of phosphorylated GSK3β(Ser9) protein was increased. Puerarin improves the learning and memory impairment by reducing the formation of Aβ, activating the GSK3β signaling pathway, inhibiting the phosphorylation of tau in APP/PS1 double transgenic mice., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)