Aim To study the effect of EA on the injury induced by hypoxia/reoxygenation in primary cultures of rat hippocampal neurons.Methods Rat hippocampal neurons in primary culture were used,and a apoptosis model was induced by hypoxia/reoxygenation.MTT assay and LDH releasing rate were used to detect the cell viability.The apoptosis rate of hippocampal neurons was analyzed by Hoechst 33258 staining,flow cytometry with AnnexinV-FITC and PI staining.Western blot was used to detect the protein expression of AKT and p-AKT.Results Compared to control group,three hours of hypoxia followed by sixteen hours of reoxygenation induced hippocampal neuronal apoptosis.EA could raise the neuronal viability and reduce apoptosis rate and the damage degree of rat hippocampal neurons.EA could increase the expressing of p-AKT.Conclusions EA has protective effects on damaged neurons,and the mechanism may be related to activating the PI3K-AKT signal transduction pathway.

Aim To observe the neurological protective effects of astragalosides(AST) on focal cerebral ischemia-reperfusion(I/R) injury in rats and to explore its possible mechanism.Methods Male SD rats received right middle cerebral artery occlusion for 120 min,and were decapitated 1,3,7,and 14 days after reperfusion.AST(40 mg?kg-1) was orally administered after I/R.Neurological deficit score was daily determined,the expressions of BDNF and p75NTR mRNA were detected by RT-PCR,and the expression of TrkB mRNA was detected by real-time PCR.Results AST reduced the neurological deficit score on days 3,increased the expression of BDNF mRNA on days 3,7 and 14,decreased p75NTR mRNA and increased TrkB mRNA on days 3 and 7.Conclusions AST improves the neurological deficits after I/R in rats.The mechanism may be related with increasing BDNF,and TrkB mRNA,and decreasing p75NTR mRNA.

OBJECTIVETo study the protective effects and mechanisms of astragaloside (AST) and astragalus saponin I (ASI) on the memory impairment in senescent rats treated by glucocorticoid (GC).

METHODY maze test was performed to determine the effects of AST and ASI on memory impairment of hydrocortisone(HC)-induced senescent rats. Using Ca2+ sensitive fluorescent indicator (Furo-2), free intracellular calcium concentration ([Ca2+]i) was measured by double wavelength fluorescence sepectrophotometer in thymocytes and hippocampal neurons induced dexamethasone (DEX). And apoptosis was detected by DNA gel electrophoresis and flow cytometry.

RESULTCompared with HC control, AST and ASI can improve the memory of the senescent rats treated by HC, lower [Ca2+]i and suppress apoptosis of thymocytes and hippocampal neurons induced by DEX.

CONCLUSIONAST and ASI can delay the aging in rats treated by HC, and its mechanism may includ lowering[Ca2+]i and suppressing the apoptosis of thymocytes and hippocampal neurons.

Aging ; drug effects ; metabolism ; pathology ; Animals ; Apoptosis ; drug effects ; Body Weight ; drug effects ; Calcium ; metabolism ; Dexamethasone ; adverse effects ; Female ; Glucocorticoids ; adverse effects ; Hippocampus ; pathology ; Intracellular Space ; drug effects ; metabolism ; Male ; Memory Disorders ; chemically induced ; metabolism ; pathology ; prevention & control ; Neurons ; drug effects ; pathology ; Rats ; Saponins ; pharmacology

Objective:To study the correlation between the time within the target range of blood glucose and the reduction of muscle mass in middle-aged and elderly patients with type 2 diabetes (T2DM).Methods:A total of 245 middle-aged and elderly T2DM patients admitted to the Second People′s Hospital of Hefei from December 2020 to December 2021 were selected. All enrolled patients wore MeiQi blood glucose monitor to obtain time in range (TIR), time above range (TAR), time below range (TBR), mean amplitude of glycemic excursions (MAGE), coefficient of variation (CV), blood glucose standard deviation (SD), largest amplitude of glycemic excursions (LAGE), which was for assessing blood sugar fluctuation. The incidence of muscle mass reduction and sarcopenia was statistically analyzed, and the differences invarious observation indicators between the muscle mass reduction group and the non muscle mass reduction group were compared. Spearman correlation analysis was used to investigate the correlation between clinical indicators and limb skeletal muscle mass index (ASMI), and logistic regression was used to analyze the influencing factors of muscle mass reduction in middle-aged and elderly T2DM patients.Results:The prevalence of muscle mass loss in 245 T2DM patients was 25.71%(63/245), and the prevalence of sarcopenia was 13.06%(32/245). There were statistically significant differences in age, gender, body mass index (BMI), blood phosphorus, homeostatic model assessment of insulin resistance (HOMA-IR), urine albumin creatine ratio (ACR), 25 hydroxyvitamin D, diabetes nephropathy (DN) patient proportion, ASMI, grip strength, and 5 sit up test times between the muscle mass reduction group and the non muscle mass reduction group (all P<0.05). The TIR of the muscle mass reduction group was lower than that of the non muscle mass reduction group, while the TAR and mean blood glucose (MG) were higher than those of the non muscle mass reduction group, with statistically significant differences (all P<0.05). ASMI was negatively correlated with age, males, and HOMA-IR (all P<0.05), but positively correlated with BMI and 25 hydroxyvitamin D (all P<0.05). ASMI was positively correlated with SD and TIR (mean P<0.05), and negatively correlated with CV, LAGE, TAR, and MG (all P<0.05). The results of univariate regression analysis showed that age, male gender, DN, and TAR were risk factors for muscle mass reduction, while BMI, 25 hydroxyvitamin D, and TIR were protective factors for muscle mass reduction (all P<0.05). After adjusting for other related factors, TIR remained a protective factor for decreased muscle mass (all P<0.05). Conclusions:TIR is an independent protective factor for muscle mass loss in middle-aged and elderly T2DM patients, and the incidence of muscle mass loss can be reduced by increasing TIR levels in clinical practice.