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目的研究和厚朴酚增强吉西他滨诱导胰腺癌细胞BXPC3凋亡的作用及机制。方法用CCK-8法检测和厚朴酚与吉西他滨对BXPC3细胞增殖的影响,用流式细胞术检测和厚朴酚及吉西他滨对BXPC3细胞凋亡的作用,用Western blot检测和厚朴酚及吉西他滨对BXPC3细胞Bcl-2、Survivin、Bax、p65、IκB-α和p-IκB-α蛋白表达的影响。结果和厚朴酚显著增强吉西他滨抑制BXPC3细胞增殖和诱导凋亡的作用,并能逆转吉西他滨诱导的Bcl-2表达上调,提高Bax/Bcl-2比值,抑制Survivin蛋白表达;和厚朴酚能够抑制核因子-κB(NF-κB)p65蛋白入核,同时抑制IκB-α磷酸化和IκB-α蛋白降解,从而逆转吉西他滨诱导的NF-κB通路的激活。结论和厚朴酚能够增强吉西他滨抑制胰腺癌细胞增殖和诱导凋亡的作用。
Objective To investigate the effects and mechanisms of honokiol on enhancing apoptosis of pancreatic cancer BXPC3 induced by gemcitabine. Methods The effects of honokiol and gemcitabine on the proliferation of BXPC3 cells were detected by CCK-8 assay. The effects of honokiol and gemcitabine on the apoptosis of BXPC3 cells were detected by flow cytometry. The levels of honokiol and gemcitabine On Bcl-2, Survivin, Bax, p65, IκB-α and p-IκB-α protein expression in BXPC3 cells. Results Honokiol significantly enhanced gemcitabine inhibition of BXPC3 cells proliferation and induction of apoptosis, and can reverse gemcitabine-induced up-regulation of Bcl-2, increased Bax / Bcl-2 ratio, inhibition of Survivin protein expression; and honokiol can inhibit Nuclear factor-κB (NF-κB) p65 enters the nucleus and inhibits IκB-α phosphorylation and IκB-α protein degradation, thereby reversing the activation of gemcitabine-induced NF-κB pathway. Conclusion Honokiol can enhance the effect of gemcitabine on the proliferation and apoptosis of pancreatic cancer cells.