Protective Effects and the Mechanismof Anemarsaponin B on Hypoxia/reoxygenation Injury Astrocytes / 中国药房

OBJECTIVE： To investigate the protective effects of anemarsaponin B on hypoxia/reoxygenation injury astrocytes and its possible mechanism. METHODS： The primary astrocytes of neonatal SD rats were cultured and identified， and then randomly divided into normal group， model group， positive control group （nimodipine， 10 μmol/L）， anemarsaponin B low-dose， medium-dose and high-dose groups （1， 10， 100 μmol/L）， respectively. Normal group and model group were given complete medium 1 000 μL. Administration group was given complete medium with relevant medicine 1 000 μL. Except for normal group， hypoxia/reoxygenation injury model was established by oxygen-glucose deprivation/reperfusion in other groups. After reoxygenation， relative release rate of lactate dehydrogenase （LDH） in cell was detected by colorimetry. MTT assay was used to detect the relative viability of the cells. The contents of aquaporin 4 （AQP-4）， IL-6， IL-1β and TNF-α in cell were measured by ELISA. RESULTS： Compared with normal group， relative release rate of LDH， the contents of AQP-4， IL-6， IL-1β and TNF-α in cell were increased significantly in model group， while relative viability of the cells were decreased significantly （P＜0.01）. Compared with model group， relative release rate of LDH， the contents of AQP-4， IL-6， IL-1β and TNF-α in cell were decreased significantly in administration groups， while relative viability of the cells were increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： Anemarsaponin B can significantly decrease cell injury degree， strengthen cell viability and protect hypoxia/reoxygenation injury astrocytes to certain extent. The effect may be related to the down-regulation of the secretion of AQP-4， IL-6， IL-1β and TNF-α.

β-caryophyllene mitigates cerebral ischemia reperfusion injury in mice by inhibiting HMGB1/TLR4/NF-κB pathway / 中国免疫学杂志

Objective:investigate the effect of β-caryophyllene(BCP)on cerebral ischemia-reperfusion(CIR)injury in mice.Methods: Mice were subjected to CIR with or without BCP(62,124,248 mg/kg).At 24 h of reperfusion,ischemic degrees were determined according to neurologic dysfunction score and cerebral infarct volume.The protein expression of Toll-like receptor(TLR)4 was measured by Western blot.Nuclear factor κB(NF-κB)p65 were measured by immunohistochemistry and Western blot.IL-1β,tumor necrosis factor-α(TNF-α)and serum high-mobility group box 1(HMGB1)levels were measured by ELISA kit.Results: Compared to the CIR group,BCP(248 mg/kg)reduced the neurological score and cerebral infarct volume.BCP reduced neuronal death in mice brain subjected to cerebral I/R.In addition,BCP also inhibited the activation of NF-κB pathway and decreased increases in TLR4,HMGB1,TNF-α,IL-1β levels by CIR(P<0.01).Conclusion: BCP protects mice brain against CIR injury,its neuroprotective mechanisms may involves HMGB1/TLR4/NF-κB pathway.