ABSTRACT
The present study aimed to systematically evaluate the efficacy and safety of Ginkgo biloba extract 50(GBE50) in the treatment of ischemic stroke. The databases including CNKI, Wanfang, VIP, SinoMed, PubMed, EMbase, and Cochrane Library were searched for randomized controlled trial(RCT) of GBE50 for the treatment of ischemic stroke reported between database inception and May 2020. The methodological quality of the included RCTs was evaluated via the Cochrane risk of bias tool. The RevMan 5.4 was used for Meta-analysis. Sixteen RCTs were included, involving 1 615 patients with acute ischemic stroke. Most of the included RCTs reported the methods of random sequence generation, but only two performed the concealment of random sequence. All RCTs failed in blinding. Two RCTs reported the information of cases lost to follow-up and drop-outs. Since the number was small, the baselines of groups remained balanced. All RCTs reported key outcomes of ischemic stroke, which made selective reporting bias in a low risk. Meta-analysis results revealed that GBE50 combined with routine therapies could effectively lower the score of the National Institutes of Health stroke scale(NIHSS) and restore cognitive function and daily activity in ischemic stroke patients. Compared with routine therapies, the combination is advantageous in treating patients with ischemic stroke. However, high-quality multicenter RCTs with large sample sizes are still required for verification.
Subject(s)
Humans , Brain Ischemia/drug therapy , Ginkgo biloba , Ischemic Stroke , Multicenter Studies as Topic , Plant Extracts , Stroke/drug therapyABSTRACT
In this study, the anti-inflammatory mechanism of Ginkgo biloba extract 50 (GBE50) and its mechanism of action on NLRP3 inflammatory corpuscles were observed by primary microglia cells. LPS/ATP was used to stimulate microglia, and the best time for stimulation and optimal concentration of GBE50 were screened. Pro-inflammatory cytokine IL-1 and TNF-α was determined by ELISA. Western blot was performed to observe the protein expression of NLRP3, ASC, caspase-1 and IL-1 in cultured primary rat microglia. Effect of GBE50 on NLRP3 inflammatory corpuscle aggregation was detected by CO-IP. GBE50 (10 mg·L⁻¹) preconditioning could significantly inhibit the expression of LPS (100 μg·L⁻¹,12 h), ATP (5 mmol·L⁻¹, 30 min) induced primary microglia corpuscle associated protein, inflammatory corpuscle aggregation, and the release of inflammatory factors IL-6 and TNF-α. These results indicated that GBE50 could inhibit the secretion of inflammatory factors after microglia activation, which is related to down regulating the protein expression and activity of NLRP3 inflammatory corpuscle.
ABSTRACT
Objective To observe the effects of Ginkgo biloba extract 50 (GBE50) on hemodynamics and myocardial tissue TNF-α pathway in rats with acute blood stasis syndrome; To discuss its mechanism of action. Methods A model of acute blood stasis syndrome was established by subcutaneous injection of epinephrine hydrochloride and ice bath. Male SD rats were divided randomly into normal group, model group and GBE50 group. After medicine was administrated by gavage for 11 days, the acute blood stasis model was established. The hemodynamic changes were observed in the next day. The expressions of TNF-α, TNFR1 and TNFR2 mRNA were detected by RT-PCR. The expressions of TNF-α, TNFR1 and TNFR2 protein were tested by radioimmunoassay and immunohistochemistry. Results The hemodynamics of the model group was lower than that of the normal group. Compared with model group, GBE50 could increase mLVSP, DP and decrease t-dp/dtmax(P<0.05). The protein expressions of TNF-α, TNFR1, and TNFR2 in GBE50 group were higher than those in model group, and TNFR2 mRNA expression increased significantly in GBE50 group (P<0.05). Conclusion GBE50 can ameliorate the decline of hemodynamics of rats with acute blood stasis syndrome, and regulate the myocardial TNF-α pathway. Increasing the expression of protective receptor TNFR2 may be one of the mechanisms of protecting cardiac function.
ABSTRACT
Objective To observe the effects of Ginkgo biloba extract 50 (GBE50) on hemodynamics and myocardial tissue TNF-α pathway in rats with acute blood stasis syndrome; To discuss its mechanism of action. Methods A model of acute blood stasis syndrome was established by subcutaneous injection of epinephrine hydrochloride and ice bath. Male SD rats were divided randomly into normal group, model group and GBE50 group. After medicine was administrated by gavage for 11 days, the acute blood stasis model was established. The hemodynamic changes were observed in the next day. The expressions of TNF-α, TNFR1 and TNFR2 mRNA were detected by RT-PCR. The expressions of TNF-α, TNFR1 and TNFR2 protein were tested by radioimmunoassay and immunohistochemistry. Results The hemodynamics of the model group was lower than that of the normal group. Compared with model group, GBE50 could increase mLVSP, DP and decrease t-dp/dtmax(P<0.05). The protein expressions of TNF-α, TNFR1, and TNFR2 in GBE50 group were higher than those in model group, and TNFR2 mRNA expression increased significantly in GBE50 group (P<0.05). Conclusion GBE50 can ameliorate the decline of hemodynamics of rats with acute blood stasis syndrome, and regulate the myocardial TNF-α pathway. Increasing the expression of protective receptor TNFR2 may be one of the mechanisms of protecting cardiac function.
ABSTRACT
Aim To observe the effect of Ginkgo biloba extract 50(GBE50)on L-type calcium current and cytosolic[Ca~(2+)]_i in ischemic guinea pig ventricular myocytes.Methods Single ventricular myocytes were isolated by enzymatic dissociation. I Ca-L was recorded by whole-cell patch clamp technique in voltage clamp mode.[Ca~(2+)]_i was detected by laser confocal micros-copy and represented by relative fluorescent intensity (FI).Results During ischemia, the peak Ca~(2+) current was reduced, and the I-U curve of I Ca-L was shifted upward.50 mg·L~(-1) GBE50 reversed the change induced by ischemia(n =6, P >0.05).After perfusing ischemic solution for 12 min, intracellular calcium concentration was increased(n =10, P <0.01).After perfusion with ischemic solution containing 50 mg·L~(-1) GBE50, the increase of intracellular calcium concentration was markedly inhibited(n =10, P >0.05).Conclusion GBE50 can reverse the decrease of I Ca-L and partially inhibit calcium overloading during ischemia.