Effects of intravenous thrombolysis with alteplase combined with edaravone on cerebral hemodynamics and T lymphocyte level in patients with acute cerebral infarction.

Our study aimed to investigate the effect of intravenous thrombolysis with alteplase and edaravone on cerebral hemodynamics and T lymphocyte level in patients harboring acute cerebral infarction.There involved a total of 118 patients with acute cerebral infarction from November 2017 to May 2019 in our hospital were randomly divided into 2 groups: the observation group (59 patients were treated with intravenous thrombolysis with alteplase combined with edaravone) and the control group (59 patients were treated with intravenous thrombolysis of alteplase). The clinical effect, neurological function, cerebral hemodynamic index, T lymphocyte level, oxygen free radical scavenging level and oxidative stress index of the 2 groups were observed and compared.Before the treatment, there were no significant differences in neurological function, cerebral hemodynamic indexes, T-lymphocyte level, oxygen free radical scavenging level and oxidative stress indexes between the 2 groups (P > .05). After the treatment, the neurological function, cerebral hemodynamic indexes, T-lymphocyte level, oxygen free radical scavenging level and oxidative stress indexes of the 2 groups were significantly improved. In addition, the observation group exerted greater beneficial effect in terms of the clinical effect, neurologic function, cerebral hemodynamic index, T lymphocyte level, oxygen free radical scavenging level and oxidative stress index than those of the control group (P < .05).The intravenous thrombolysis with alteplase and edaravone is effective in the treatment of acute cerebral infarction, which also provides better results in terms of improving the clinical efficacy and prognosis of patients and might be an alternative option for clinical practice.

Effects of oxiracetam combined with ginkgo biloba extract in the treatment of acute intracerebral hemorrhage: A clinical study.

PURPOSE: The present clinical study was conducted to investigate the effect of oxiracetam combined with ginkgo biloba extract in treating patients with acute intracerebral hemorrhage. METHODS: Ninety-eight patients with acute cerebral hemorrhage admitted to our hospital were divided into three groups. The differences of brain edema and cerebral hemorrhage were compared between the three groups after 1 and 2 weeks of treatment, and the recovery of neurological function, serum inflammatory factors, AQP-4, MMP-9, cognitive function, activities of daily living, and adverse reactions were compared between the three groups after 2 weeks of treatment. RESULTS: There was no significant difference among the three groups before treatment (p > .05). After treatment, the recovery of neurological function, serum inflammatory factors, AQP-4, MMP-9 levels, cognitive function, and activities of daily living were improved. Among them, the neurological function recovery, serum inflammatory factors, AQP-4, MMP-9 levels, cognitive function, and activities of daily living in the combined treatment group and the control group elicited greater results than those in the routine group. The results of the combined treatment group showed the most significant difference (p < .05). The concentration of IL-6 decreased from 135.98 ± 12.54 to 91.83 ± 7.69 pg/ml, AQP-4 from 227.55 µg/L ± 21.06 to 114.31 ± 9.22 µg/L, and MMP-9 from 172.39 ± 9.81 to 94.98 ± 5.01 ng/ml. In addition, the neurological function recovery, the levels of serum inflammatory factors, cognitive function, and activities of daily living in the combined treatment group were better than those in the control group (p < .05). The mean score of MRS in the combined treatment group decreased from 3.36 ± 0.98 at admission to 1.91 ± 0.38. CONCLUSION: Oxiracetam combined with Ginkgo biloba extract in the treatment of acute cerebral hemorrhage has a significant improvement effect.

Significant association of BDNF rs6265 G>A polymorphism with susceptibility to epilepsy: a meta-analysis.

INTRODUCTION: Previously published articles have suggested that BDNF rs6265 G>A polymorphism is a potential risk factor for epilepsy. However, the results were not consistent. METHODS: We conducted a meta-analysis to explore the association between BDNF rs6265 G>A polymorphism and epilepsy risk. Four online databases were searched, and related studies were reviewed from their inception up to June 20, 2017. ORs and corresponding 95% CIs were used to calculate the associations of each genetic model. Overall, 10 case-control publications involving 9,512 subjects were included in this meta-analysis. RESULTS: Significant associations were found between BDNF rs6265 G>A polymorphism and epilepsy (A vs G: OR=0.88, 95% CI=0.83-0.94, P<0.01, I2=0%; GA vs GG: OR=0.88, 95% CI=0.79-0.97, P=0.01, I2=0%; AA vs GG: OR=0.79, 95% CI=0.70-0.90, P<0.01, I2=0%; GA+AA vs GG: OR=0.85, 95% CI=0.77-0.94, P<0.01, I2=0%; AA vs GG+GA: OR=0.85, 95% CI=0.76-0.95, P=0.01, I2=0%). Subgroup analysis also showed similar results in an Asian population. CONCLUSION: Our meta-analysis indicated that BDNF rs6265 G>A polymorphism might be involved in epilepsy susceptibility, especially in the Asian population.

Hsa_circ_0007534/miR-761/ZIC5 regulatory loop modulates the proliferation and migration of glioma cells.

Increasing evidences demonstrate the essential roles of circular RNAs (circRNAs) in human cancers. However, the study about the functions of circRNAs in glioma remains very limited. In the present study, we found that circRNA hsa_circ_0007534 was highly expressed in glioma tissues compared to normal brain tissues. Furthermore, we found that knockdown of hsa_circ_0007534 significantly inhibited the proliferation and migration of glioma cells. In mechanism, we showed that hsa_circ_0007534 could sponge miR-761 to repress its availability in glioma cells. We found that inhibition of miR-761 could rescue the suppressed proliferation and migration of glioma cells by hsa_circ_0007534 knockdown. Moreover, we explored the downstream mechanism and found that ZIC5 was a target of miR-761. We showed that hsa_circ_0007534 promoted the expression of ZIC5 by inhibiting miR-761 in glioma cells. And restoration of ZIC5 expression significantly reversed the effects of hsa_circ_0007534 knockdown on glioma cell proliferation and migration. In summary, our results demonstrated that hsa_circ_0007534 serves as an oncogene in glioma via promoting ZIC5 expression by repressing miR-761 availability. Our results suggested that hsa_circ_0007534/miR-761/ZIC5 regulatory loop might be a promising therapeutic target for glioma treatment.

Inhibition of microRNA-34a protects against propofol anesthesia-induced neurotoxicity and cognitive dysfunction via the MAPK/ERK signaling pathway.

AIM: To investigate the protective effect of microRNA-34a (miR-34a) on propofol-induced neurotoxicity and cognitive dysfunction. METHODS: After SH-SY5Y cells were treated with propofol to induce neurotoxicity, microRNA-34a mimics and inhibitors were transfected into the cells. The expression of apoptosis-related genes and the proteins were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot. Sprague-Dawley (SD) rats received intraperitoneal injections of propofol, and were treated with microRNA-34a mimics and lentivirus-mediated microRNA-34a inhibitors. The Morris water maze (MWM) test was used to detect changes in motor function. RESULTS: Propofol anesthesia had an adverse effect on cell survival due to the increased expression of apoptosis-related genes such as cleaved caspase-3/8 and Bax, which was accompanied by reduced expression of ERK1/2, pERK1/2, and phosphorylated NF-kappaB p65 both in vivo and in vitro. Unexpectedly, microRNA-34a was upregulated after propofol treatment, and the inhibitors protected the SH-SY5Y cells from propofol-induced apoptosis. The microRNA-34a inhibitor suppressed the apoptosis-induced effects of propofol. This protection may have been partly diminished by PD98059, a MAPK kinase inhibitor. MicroRNA-34a inhibited or reverted the reduced expression of ERK1/2 and upregulated the expression of p-CREB significantly and specifically. Additionally, the microRNA inhibitors improved the learning and memory functions of animals suffering from neurologic impairment due to propofol treatment and reduced cell apoptosis in the hippocampus. CONCLUSION: microRNA-34a could improve anesthesia-induced cognitive dysfunction by suppressing cell apoptosis and recovering the expression of genes associated with the MAPK/ERK signaling pathway.