Abstract In this study, the synergistic effects of jujube polysaccharide (JP) and flavonoid (JF) on aging mice were investigated. Sub-acutely aging mouse models were established using D-galactose. Eighty experimental mice were randomly assigned to normal, model, vitamin C (200 mg/kg), JP (200 mg/kg), JF (200 mg/kg) and JP + JF (low (100 mg/kg), medium (200 mg/kg), and high-dose (300 mg/kg)) groups (10 mice in per group). After 35 days, the physiological aging indices of mice were measured. JP and JF displayed significantly positive synergistic antiaging effects. Compared with an aging model control group, groups administered JP and JF showed increased indices for the thymus and spleen and significantly increased activities of SOD and GSH-PX in the heart, liver, spleen, and brain (R2 > 0.99, P < 0.01; R2 > 0.98, P < 0.01). The contents of MDA in heart, liver, spleen, brain and serum were significantly decreased (R2 > 0.95, P < 0.01), while those of HYP in skin and serum were significantly increased. The concentrations of neurotransmitters (NE, DA, 5-HT, 5-HIAA) in the brain and serum of mice were significantly increased (P < 0.01). These results indicated that JP and JF acted not only on relevant tissues or organs of mice, but on all body systems.

This study aimed to explore the effect of intravenous thrombolysis with alteplase on clinical efficacy, inflammatory factors, and neurological function in patients with acute cerebral infarction. A total of 120 patients with acute cerebral infarction were divided into two groups by the random number table method, with 60 patients in each group: observation group (intravenous thrombolysis with alteplase) and control group (intravenous thrombolysis with batroxobin). The clinical efficacy after a 14-day treatment was observed. Serum C-reactive protein (CRP), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), CD62p, GMP-140, and neuron-specific enolase (NSE) were measured. Scores of National Institutes of Health Stroke Scale (NIHSS), Mini-Mental State Examination (MMSE), and Montreal Cognitive Assessment (MoCA) were determined. The total effective rate in the observation group was 81.67%, which was higher than the 61.67% in the control group (P<0.05). The improvement of inflammatory factors (CRP, TNF-α, IL-6, CD62p, GMP-140, and NSE), NIHSS, MMSE, and MoCA in the observation group was superior to that in the control group (all P<0.05). The modified Rankin scale at three months after hospital discharge in the observation group was lower than that in the control group (P<0.01). Intravenous thrombolysis with alteplase for acute cerebral infarction can enhance the clinical efficacy, alleviate inflammatory response and brain injury, and improve cognitive function, which is worthy of further clinical application and study.

PURPOSE: To investigate the anticancer activity of ellagic acid (EA) in U251 human glioblastoma cells and its possible molecular mechanism. METHODS: The cells were treated with EA at various concentrations for different time periods. Cell viability and cell proliferation were detected by cell counting kit-8(CCK-8) assay and live/dead assay respectively. Cell apoptosis were measured with Annexin V-FITC/PI double staining method by flow cytometry and Mitochondrial membrane potential assay separately. Cell cycle was measured with PI staining method by flow cytometry. The expressions of Bcl-2, Survivin, XIAP, Caspase-3, Bax, JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38, DR4, DR5, CHOP and GRP78-related proteins were detected by western blot after EA treatment. RESULTS: Cell viability and proliferation of glioblastoma cells treated with EA were significantly lower than the control group. EA caused robust apoptosis of the glioblastoma cells compared to the control group. EA significantly decreased the proportion at G0/G1 phases of cell cycling accompanied by increased populations at S phase in U251 cell lines. And the expressions of anti-apoptotic proteins were dramatically down-regulated. CONCLUSION: Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38). EA also caused significant increase in the expressions of CHOP and GRP78. Our findings suggest that EA would be beneficial for the treatment of glioblastoma.