PMID- 29710487 OWN - NLM STAT- MEDLINE DCOM- 20180917 LR - 20220408 IS - 1950-6007 (Electronic) IS - 0753-3322 (Linking) VI - 99 DP - 2018 Mar TI - Protective effect and mechanism of ginsenoside Rg1 in cerebral ischaemia-reperfusion injury in mice. PG - 876-882 LID - S0753-3322(17)36538-1 [pii] LID - 10.1016/j.biopha.2018.01.136 [doi] AB - BACKGROUND: Ginsenoside Rg1 is regarded as one of main bioactive compounds responsible for pharmaceutical actions of ginseng with little toxicity and has been shown to have possibly neuroprotective effects. However, the mechanism of its neuroprotection for acute ischemic stroke is still elusive. The purpose of present study is thus to assess the neuroprotective effects of the ginsenoside Rg1 against neurological injury in a mice model of cerebral ischemia/reperfusion (I/R), and then to explore the mechanisms for these neuroprotective effects. METHODS: Mices were pretreated with ginsenoside Rg1 20,40?mg?kg(?1)?d(?1), ig, for 7d, respectively, then subjected to cerebral ischenmia (middle cerebral artery occlusion) for 2?h and reperfusion for 22?h. The infarct volume and the neurological deficit were determined by TTC staining and Longa?s scoring, respectively. The protein expression of brain-derived neurotrophic factor (BDNF) was analyzed by Immunohistochemistry and Western blot, respectively. Interleukin-1? (IL-1?), tumor necrosis factor alpha (TNF-?) and interleukin-6 (IL-6) expression in serum was measured by ELISA kit. High-performance liquid chromatography (HPLC) was used to explore the contents of Glu and Asp. RESULTS: Compared with the ischemia/reperfusion group, ginsenoside Rg1 40?mg/kg group has significantly reduced infarct volume, neurological deficit scores (P?