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Aim This investigation was to identify whether Janusactivated kinase 2(JAK2) and mitogenactivated protein kinase (MAPK) pathways were involved in the inhibitory effect of berberine hydrochloride (BER) on gastric cancer cell proliferation and IL8 expression in vitro and in vivo.Methods CCK8 assay was used to assess the cell proliferation.IL8 production was determined by ELISA and qPCR assay.Molecular pathways involved were evaluated by ELISA and westernblotting methods.Results BER timeand dosedependently inhibited the proliferation of MGC 803 and AGS cells.It also suppressed tumor growth in nude mice xenografted with MGC 803 cells.In addition, BER reduced interleukin8 (IL8) secretion of AGS cells as well as MGC 803 cells both in vitro and in vivo.Further study disclosed that inactivation of JAK2, p38 MAPK, ERK1/2and JNK by BER contributed to the decreased proliferation and tumor growth as well as IL8 expression in gastric cancer.Although there was no significantly synergistic inhibitory effect between BER and evodiamine on gastric cancer cell proliferation and tumor growth, BER could counteract the upregulation of IL8 induced by evodiamine in vitro and vivo.Conclusions Our results suggested that BER might be an efficient and safe drug candidate for treating gastric cancer through JAK2 and MAPK pathways.