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纸质出版:2014
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陈璐,何文华,朱萱,李弼民,张焜和,施凤,张新华.熊果酸对肝星状细胞NADPH 氧化酶-Hedgehog 信号通路的影响[J].陆军军医大学学报(原第三军医大学学报),2014,36(05):427-431.
Chen Lu,He Wenhua,Zhu Xuan,Li Bimin,Zhang Kunhe,Shi Feng,Zhang Xinhua.Ursolic acid suppressed NADPH oxidase-Hedgehog signaling pathway in hepatic stellate cells in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(05):427-431.
陈璐,何文华,朱萱,李弼民,张焜和,施凤,张新华.熊果酸对肝星状细胞NADPH 氧化酶-Hedgehog 信号通路的影响[J].陆军军医大学学报(原第三军医大学学报),2014,36(05):427-431. DOI:
Chen Lu,He Wenhua,Zhu Xuan,Li Bimin,Zhang Kunhe,Shi Feng,Zhang Xinhua.Ursolic acid suppressed NADPH oxidase-Hedgehog signaling pathway in hepatic stellate cells in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(05):427-431. DOI:
目的 探讨熊果酸(ursolic acid,UA)对大鼠肝星状细胞(HSC-T6)的NADPH氧化酶(NOX)-Hedgehog(Hh)信号通路的影响。 方法 将处于对数生长期的HSC-T6细胞分为6组:正常对照组、瘦素组(100 ng/mL)、熊果酸自身对照组(50 μmol/L)、DPI自身对照组(20 μmol/L)、熊果酸干预组(瘦素+熊果酸)、DPI干预组(瘦素+DPI)。在药物作用12 h后,提取总RNA,采用RT-PCR法检测Shh、Smo、Gli1/2的表达;药物作用HSC-T6 细胞24 h后,提取总蛋白,采用Western blot分别检测Rac1和Gli2的表达;药物作用12、24、48 h后,采用MTT法检测HSC-T6细胞的增殖情况。 结果 RT-PCR分析显示,瘦素刺激HSC-T6细胞12 h后Smo mRNA表达较正常对照组升高(
P
0.05);Shh、Gli2 mRNA表达稍高于正常对照组,但差异无统计学意义(
P
0.05); 熊果酸干预后Shh、Smo和Gli2 mRNA表达明显低于瘦素组及正常对照组(均
P
0.05);瘦素对HSC-T6细胞Gli1 mRNA的表达无影响,而熊果酸及DPI干预也不影响HSC-T6细胞Gli1 mRNA 的表达。瘦素刺激HSC-T6细胞24 h后,Rac1和 Gli2蛋白的表达较正常对照组升高(
P
0.01);熊果酸干预后Rac1和Gli2蛋白的表达明显低于瘦素组(
P
0.01)。MTT分析显示瘦素促进HSC-T6细胞增殖,熊果酸干预12 h后HSC-T6细胞的生长抑制率均显著高于瘦素组(
P
0.01),随着作用时间延长,熊果酸对细胞生长的抑制作用进一步增强。 结论 熊果酸能抑制瘦素诱导的HSC-T6细胞Hh信号通路Shh、Smo、Gli2 mRNA和 Gli2蛋白表达。熊果酸通过抑制NOX亚基Rac1蛋白表达进而抑制Hh信号通路可能是它抑制肝星状细胞生长增殖的机制之一。
Objective To determine the effect of ursolic acid (UA) on NADPH oxidase (NOX)- Hedgehog (Hh) signaling pathway in hepatic stellate cells(HSCs). Methods Culture-
activated HSC-T6 cells were divided into 6 groups: normal control group
leptin group (100 ng/mL)
UA group (50 μmol/L)
NOX inhibitor DPI (20 μmol/L) group
and the 2 intervention groups pretreated with UA or DPI followed by stimulation with leptin for different times. The mRNA expression of Shh
Smo and Gli1/2 was detected in above cells after 12 hours’ treatment by RT-PCR. The protein expression of Rac1 and Gli2 were analyzed in the cells in 24 h of treatment by Western blotting. The proliferation of HSC-T6 cells was detected in 12
24 and 48 h after treatment by MTT assay. Results RT-PCR analysis showed that Smo mRNA expression was increased when leptin stimulated HSC-T6 cells for 12 h (
P
0.05). The expression of Shh and Gli2 mRNA was also increased compared with normal control group
but without significant difference. UA pretreatment significantly down-regulated the mRNA expression of Shh
Smo and Gli2 compared with control and leptin group (all
P
0.05). Leptin
UA and DPI had no effect on Gli1 mRNA expression. The protein expression of Rac1 and Gli2 was increased when leptin stimulated HSC-T6 cells for 24 h (
P
0.01). UA pretreatment significantly down-regulated Rac1 and Gli2 protein expression compared with leptin group (all
P
0.01). MTT assay showed that leptin promoted the proliferation in HSC-T6 cells. After 12 hours’ pretreatment with UA
the cell growth was inhibited significantly than in leptin treated cells (
P
0.01) in a time-dependent manner. Conclusion UA inhibits the expression of Shh
Smo
Gli2 mRNA and down-regulates the expression of Gli2 protein in HSC-T6 cells. One mechanism of UA inhibiting cell proliferation is probably via its inhibiting NOX subunit Rac1 and then NOX-Hh signaling pathway.
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