本文關(guān)鍵詞： 鹽酸小檗堿 α煙堿型乙酰膽堿受體 HepG細(xì)胞 胰島素抵抗　出處：《中國(guó)糖尿病雜志》2017年05期 　論文類型：期刊論文

【摘要】：目的探討鹽酸小檗堿作用α7煙堿型乙酰膽堿受體(nAchR)與改善氓的分子機(jī)制。方法建立IR HepG2細(xì)胞模型,用鹽酸小檗堿(BBR)、煙堿(NIC)干預(yù),并設(shè)正常對(duì)照(NC)組和模型組。用現(xiàn)代分子生物學(xué)檢測(cè)細(xì)胞培養(yǎng)液葡萄糖消耗量、乙酰膽堿酯酶(AchE)、乙酰膽堿(Ach)、白介素-6(Ⅱ-6)、核因子-κB(NF-κB p65)、IκB激酶βSer181(ⅡKKβSer181)、α7nAchR、磷酸肌醇3激酶(PI3K)、葡萄糖轉(zhuǎn)運(yùn)因子4(GluT4)等相關(guān)指標(biāo),用熒光標(biāo)記方法檢測(cè)細(xì)胞攝取葡萄糖的熒光強(qiáng)度。結(jié)果葡糖糖消耗量NC組、HepG2細(xì)胞模型組、BBR組和NIC組依次為(25.33±0.77)mmol/L、(11.95±1.94)mmol/L、(16.85±0.33)mmol/L和(16.27±1.09)mmol/L。細(xì)胞內(nèi)2-NBDG(熒光標(biāo)記葡萄糖)熒光強(qiáng)度增強(qiáng),NC組、HepG2細(xì)胞模型組、BBR組和NIC組依次為(118.17±14.30)、(92.33±9.35)、(120.50±26.26)和(127.67±16.07)。BBR能抑制細(xì)胞AchE活性,抑制率為53%,NIC對(duì)AchE活性無(wú)影響。BBR和NIC能激活α7nAchR,抑制IKKβSer181和NF-κBp65的表達(dá),降低炎性細(xì)胞因子IL-6,上調(diào)PI3K、GluT4,與HepG2細(xì)胞模型組比較,差異有統(tǒng)計(jì)學(xué)意義(P0.05或P0.01)。結(jié)論 BBR可能通過(guò)抑制AchE活性以激活α7nAchR,從而抑制IKKβSer181、NFκB p65和炎癥因子IL-6的表達(dá),促進(jìn)PI3K、GluT4上調(diào),發(fā)揮其改善IR、降低葡萄糖的作用。NIC雖不能抑制AchE活性,但它是特異性激動(dòng)劑,可直接激活α7nAchR。
[Abstract]:Objective to investigate the molecular mechanism of berberine hydrochloride acting on 偽 7 nicotinic acetylcholine receptor (偽 7 nicotinic acetylcholine receptor) and its amelioration. Methods IR HepG2 cell model was established and treated with berberine hydrochloride or nicotinic acid. The glucose consumption of cell culture medium was measured by modern molecular biology. Acetylcholinesterase acetylcholinesterase (ache), acetylcholine (ache), interleukin-6 (鈪，

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