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Genmeng Yang,Juan Li,Yanxia Peng,Baoyu Shen,Yuanyuan Li,Liu Liu,Chan Wang,Yue Xu,Shucheng Lin,Shuwei Zhang,Yi Tan,Huijie Zhang,Xiaofeng Zeng,Qi Li,Gang Lu 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.3
This study investigates the effects of ginsenoside Rb1 (GsRb1) on methamphetamine (METH)-induced toxicity in SH-SY5Y neuroblastoma cells and METH-induced conditioned place preference (CPP)in adult Sprague-Dawley rats. It also examines whether GsRb1 can regulate these effects through theNR2B/ERK/CREB/BDNF signaling pathways. Methods: SH-SY5Y cells were pretreated with GsRb1 (20 mM and 40 mM) for 1 h, followed by METHtreatment (2 mM) for 24 h. Rats were treated with METH (2 mg/kg) or saline on alternating days for 10days to allow CPP to be examined. GsRb1 (5, 10, and 20 mg/kg) was injected intraperitoneally 1 h beforeMETH or saline. Western blot was used to examine the protein expression of NR2B, ERK, P-ERK, CREB, PCREB, and BDNF in the SH-SY5Y cells and the rats' hippocampus, nucleus accumbens (NAc), and prefrontal cortex (PFC). Results: METH dose-dependently reduced the viability of SH-SY5Y cells. Pretreatment of cells with 40mM of GsRb1 increased cell viability and reduced the expression of METH-induced NR2B, p-ERK, p-CREBand BDNF. GsRb1 also attenuated the expression of METH CPP in a dose-dependent manner in rats. Further, GsRb1 dose-dependently reduced the expression of METH-induced NR2B, p-ERK, p-CREB, andBDNF in the PFC, hippocampus, and NAc of rats. Conclusion: GsRb1 regulated METH-induced neurotoxicity in vitro and METH-induced CPP through theNR2B/ERK/CREB/BDNF regulatory pathway. GsRb1 could be a therapeutic target for treating METHinduced neurotoxicity or METH addiction.