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Objective To explore the effects of gross saponins of Tribulus terrestris L.on inflammatory reaction and permeability of blood-brain barrier in rats following cerebral ischemia-reperfusion injury and their potential mechanisms. Methods Sixty SD rats were divided into sham operation group,model control group,gross saponins of Tribulus terrestris L.at low-dose (10 mg?kg-1 )and high-dose groups(30 mg?kg-1 ).Cerebral ischemia -reperfusion model was established with suture emboli method in middle cerebral artery of rats.Neural injury scores,the contents of Evans blue ( EB) and myeloperoxidase( MPO) activities in rat brain were measured 24 hours after the cerebral reperfusion post 2 h ischemia.Content of tumor necrosis factor-α (TNF-α) in rat brain was detected by ELISA; expression levels of matrix metalloproteinase-9(MMP-9) in rat brain was determined by Western blot. Results Compared to the model control group,the neurological deficit scores were significantly decreased(P<0.05),MPO activities and EB contents decreased(P< 0.05 or P< 0.01) in the treatment groups.The expression levels of TNF-α were significantly lower in the treatment groups(0.760±0.110) mg?g-1 and (0.670±0.073) mg?g-1 compared to (0.920±0.128) mg?g-1 in the model control group ( P< 0.05 or P< 0.01). The MMP-9 expression levels were (1.770± 0.181)% and(1.480±0.146)%,significantly lower than(2.200±0.186)% in the model control group(P<0.01). Conclusion Gross saponins of Tribulus terrestris L. exert neuroprotective effects on cerebral ischemia-reperfusion injury in rats through inhibiting the inflammatory reaction and decreasing the permeability of blood-brain barrier,which may be associated with the decrease of the TNF-α content and downregulation of the MMP-9 expression.
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Objective To investigate the protective effct of Panax quinquefolium saponins from steams and leaves(PQS)on focal cerebral ischemia injury in rats and its mechanisms. Methods Wistar rats were randomly divided into sham operation group,model control group,nimodipine group and two PQS groups,in which PQS of 100 and 50 mg/kg was intragastrically administered. Focal cerebral ischemia model was established by middle cerebral artery occlusion (MCAO)in rats, via string ligation of artetia carotis interna. The content of malondicldehy de(MDA) was determined by thibabituric acid ( TBA ) test, the activity of lactate dehydrogenase ( LDH ), superoxide dismutase (SOD)and the content of lactic acid(LA) were detected by chemical colorimetry test in cerebral tissues. Results PQS( 100,50mg/kg)could significantly decrease the content of LA、MDA and increase the activity of LDH、SOD. Conclusion The protective mechanism of PQS on focal cerebral ischemia injury may be related to reduce acidosis, anti-free radical and resist oxidative damage.
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Objective To investigate the anti-fatigue effect of complex bear gall agent in mice.Methods Different dose of complex bear gall agent(4.4ml/kg、6.6ml/kg、13.2rml/kg)were given to mice by intragastric administration. The time of climbing-pole and loaded-swimming, hepatic glycogen content, serum urea nitrogen,lactic acid and lactate dehydrogenase of mice after swim were observed. Results The experiments indicated that complex bear gall agent could greatly increase the time of loaded-swimming and climbing Pole,increase the hepatic glycogen content and serum lactate dehydrogenase activity ,decrease serum urea nitrogen and blood lactic acid content in mice. Conclusion Complex bear gall agent had a significant anti-fatigue effect.