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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation of dynorphin-mediated κ-opioid receptor and downregulation of substance P-mediated neurokinin 1 receptor

Fig. 3

Role of κ-opioid receptor in GRe-mediated modulation of prodynorphin and substance P. Experimental design for determining whether κ-opioid receptor is involved in GRe-mediated effects against dopaminergic toxicity induced by MA; mice received Nor-B by two times (3 and 1.5 h) before MA treatment. Mice received ginsenoside Re twice a day for seven consecutive days (i.e., 5 days before and 1 day after MA) (a). Effect of GRe on MA-induced decrease in prodynorphin mRNA expression in the striatum of mice (b). Effects of κ-opioid receptor antagonist Nor-B on GRe-mediated pharmacological activity against MA-induced increases in substance P (SP)-immunoreactivity (c) and substance P mRNA expression (d) in the substantia nigra (SN) of DYN KO mice. Sal = saline, MA = methamphetamine 35 mg/kg, i.p., GRe = ginsenoside Re 20 mg/kg, i.p., Nor-B = nor-binaltorphimine 3 or 6 mg/kg, i.p., WT = wild-type mice, DYN KO = prodynorphin knockout. Each value is the mean ± SEM of six animals [two-way ANOVA (B) or one-way ANOVA (C and D) followed by Fisher’s LSD pairwise comparisons]. Scale bar = 100 μm

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