二氧化硫及其衍生物對(duì)大鼠心肌細(xì)胞膠原蛋白表達(dá)的影響
發(fā)布時(shí)間:2018-11-20 21:40
【摘要】:以100μmol·L~(-1)亞硫酸氫鈉對(duì)H9C2心肌細(xì)胞染毒不同時(shí)間(3,6,12,24 h),采用Wistar大鼠作為模型進(jìn)行整體動(dòng)物染毒,SO_2組動(dòng)式吸入SO_2(7 mg·m~(-3))28 d,每天4 h;SO~(2+)NALC(N-乙酰半胱氨酸)組吸入同樣條件的SO_2,且自SO_2染毒之日起隔天腹腔注射50 mg·kg-1(b.w.)NALC,對(duì)照組吸入新鮮空氣并注射生理鹽水.測(cè)定大鼠心臟組織和H9C2細(xì)胞內(nèi)ROS含量;采用熒光定量PCR和Western blot分析I型膠原(Col1a1)和III型膠原(Col3a1)的mRNA轉(zhuǎn)錄和蛋白表達(dá)水平.結(jié)果顯示SO_2及其衍生物引起的氧化應(yīng)激顯著增加了活性氧(ROS)的產(chǎn)生;SO_2及其衍生物不能誘導(dǎo)大鼠心臟組織和H9C2細(xì)胞中Col1a1和Col3a1 mRNA轉(zhuǎn)錄水平的顯著改變,但Col1a1和Col3a1的蛋白表達(dá)水平顯著升高;同時(shí)NALC可減少心臟組織中ROS的產(chǎn)生,有效抑制SO_2吸入后Col1a1和Col3a1蛋白表達(dá)的上升.提示SO_2吸入后可能通過(guò)產(chǎn)生ROS最終導(dǎo)致膠原蛋白表達(dá)的增加.
[Abstract]:H9C2 cardiomyocytes were exposed to 100 渭 mol L ~ (-1) bisulfite sodium at different time (3 ~ 6 ~ 12 ~ (-1) h),). SO_2 group was exposed to SO_2 (7 mg m ~ (-3) for 28 days by dynamic inhalation of SO_2 (7 mg m ~ (-3). 4 hours per day; SO~ (2) NALC (N-acetylcysteine) group inhaled the same SO_2, and injected 50 mg kg-1 (B. w.) NALC, control group with fresh air and normal saline every other day from the day of SO_2 exposure. The levels of mRNA transcription and protein expression of type I collagen (Col1a1) and III type collagen (Col3a1) were determined by fluorescence quantitative PCR and Western blot. The results showed that oxidative stress induced by SO_2 and its derivatives significantly increased the production of reactive oxygen (ROS). SO_2 and its derivatives could not induce significant changes of Col1a1 and Col3a1 mRNA transcription levels in rat heart tissues and H9C2 cells, but the expression levels of Col1a1 and Col3a1 were significantly increased. At the same time, NALC can reduce the production of ROS in heart tissue and inhibit the increase of Col1a1 and Col3a1 protein expression after SO_2 inhalation. These results suggest that SO_2 inhalation may result in an increase in collagen expression through the production of ROS.
【作者單位】: 山西大學(xué)環(huán)境與資源學(xué)院;廣州市環(huán)境暴露與健康重點(diǎn)實(shí)驗(yàn)室暨南大學(xué)環(huán)境學(xué)院;
【基金】:國(guó)家自然科學(xué)基金(No.21007036) 廣州市環(huán)境暴露與健康重點(diǎn)實(shí)驗(yàn)室開(kāi)放基金(No.GZKLEEH201612) 環(huán)境化學(xué)與生態(tài)毒理學(xué)國(guó)家重點(diǎn)實(shí)驗(yàn)室開(kāi)放基金資助項(xiàng)目(No.KF2016-17)~~
【分類(lèi)號(hào)】:X51;R54
本文編號(hào):2346118
[Abstract]:H9C2 cardiomyocytes were exposed to 100 渭 mol L ~ (-1) bisulfite sodium at different time (3 ~ 6 ~ 12 ~ (-1) h),). SO_2 group was exposed to SO_2 (7 mg m ~ (-3) for 28 days by dynamic inhalation of SO_2 (7 mg m ~ (-3). 4 hours per day; SO~ (2) NALC (N-acetylcysteine) group inhaled the same SO_2, and injected 50 mg kg-1 (B. w.) NALC, control group with fresh air and normal saline every other day from the day of SO_2 exposure. The levels of mRNA transcription and protein expression of type I collagen (Col1a1) and III type collagen (Col3a1) were determined by fluorescence quantitative PCR and Western blot. The results showed that oxidative stress induced by SO_2 and its derivatives significantly increased the production of reactive oxygen (ROS). SO_2 and its derivatives could not induce significant changes of Col1a1 and Col3a1 mRNA transcription levels in rat heart tissues and H9C2 cells, but the expression levels of Col1a1 and Col3a1 were significantly increased. At the same time, NALC can reduce the production of ROS in heart tissue and inhibit the increase of Col1a1 and Col3a1 protein expression after SO_2 inhalation. These results suggest that SO_2 inhalation may result in an increase in collagen expression through the production of ROS.
【作者單位】: 山西大學(xué)環(huán)境與資源學(xué)院;廣州市環(huán)境暴露與健康重點(diǎn)實(shí)驗(yàn)室暨南大學(xué)環(huán)境學(xué)院;
【基金】:國(guó)家自然科學(xué)基金(No.21007036) 廣州市環(huán)境暴露與健康重點(diǎn)實(shí)驗(yàn)室開(kāi)放基金(No.GZKLEEH201612) 環(huán)境化學(xué)與生態(tài)毒理學(xué)國(guó)家重點(diǎn)實(shí)驗(yàn)室開(kāi)放基金資助項(xiàng)目(No.KF2016-17)~~
【分類(lèi)號(hào)】:X51;R54
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