12h</sup> 或 24h 。實(shí)驗(yàn)分為對(duì)照組、TGF-β1組和TG F?β1+Rg1 組。采用實(shí)時(shí)熒光定量PCR檢測(cè)RAs反應(yīng)性指標(biāo)膠質(zhì)纖維酸性蛋白(Gfap)、S100,炎性因子白細(xì)胞介素 1β(IL-Iβ) 、腫瘤壞死因子 α(TNF- α )、誘導(dǎo)型一氧化氮合酶(iNOS),A1型As標(biāo)志物Gbp2 .H2–T23 ,及A2型As標(biāo)志物 S100AIO?Ptx3 的mRNA表達(dá)。應(yīng)用Western blotting 檢測(cè)GFAP和iNOS的蛋白表達(dá)變化。結(jié)果應(yīng)用人參皂苷 Rg1 可顯著降低RAs中Gfap、S10O、iNOS、TNF-a 和 IL–Iβ 的mRNA表達(dá) (F=11.09~136.70,q=6.43~16.01,P<0.05) ,及GFAP和iNOS的蛋白表達(dá) (F=8.67,7.66,q=6.80,5.36,P<0.05) 。與對(duì)照組相比較, TGF-β1+Rg1 組A1型As標(biāo)志物Gbp2、 H2–T23 顯著降低 (F=61.94,18.46,q=13.95,5.58,P<0.05) ,而A2型As標(biāo)志物 S100A10?Ptx3 顯著升高(F=25.46、31.11, q=7.70,10.65,P<0.01) 。與TGF-β1組相比, TGF-β1+Rg1 組A1型As標(biāo)志物Gbp2、H2-T23顯著下降 ?F=61.94,18.46,q=13.29,8.45,P<0.01) ,而A2型As標(biāo)志物 S100AIO?Ptx3 變化不明顯。結(jié)論人參皂苷 Rg1 可抑制TGF- <sub>?β1</sub> 誘導(dǎo)的RAs反應(yīng)性特性,并促進(jìn)As由A1型向A2型轉(zhuǎn)變。-龍?jiān)雌诳W(wǎng)" />

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人參皂苷Rg1對(duì)TGF-β1誘導(dǎo)的星形膠質(zhì)細(xì)胞反應(yīng)性特性及細(xì)胞表型的影響

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[關(guān)鍵詞]人參皂苷 Rg1 ;星形膠質(zhì)細(xì)胞;轉(zhuǎn)化生長(zhǎng)因子β1;表型[中圖分類(lèi)號(hào)]R741;R284 [文獻(xiàn)標(biāo)志碼]A [文章編號(hào)] 2096-5532(2025)03-0345-05doi:10.11712/jms.2096-5532.2025.61.097 [開(kāi)放科學(xué)(資源服務(wù))標(biāo)識(shí)碼(OSID)][網(wǎng)絡(luò)出版] https://link.cnki.net/urlid/37.1517.R.20250730.1031.003; 2025-07-3014:11:53

Effect of ginsenosideRg1onTGF-β1-induced reactivityand phenotypeof astrocytesHULirong,CHEN Wenfang,ZHENG Yangyang (Department of Physiologyand Pathophysiology,Schoolof Basic Medicine,Qingdao University,Qingdao 266071,China)

[Abstract]ObjectiveTo investigate the efectof ginsenosideRglonthereactivecharacteristicsand phenotypic transformationofastrocytes(As)inducedbytransforminggrowthfactor-beta1(TGF-β1).MethodsAs wereisolatedfromthecerebral cortex of neonatal Sprague-Dawleyratsandwereinducedintoreactiveastrocytes(RAs)byTGF-βl,andthenRAsweretreated with ginsenoside Rg1 for 12 or 24 hours. The experiment was divided into control group,TGF-βl group,and TGF- group. Quantitative real-time PCR was used to measure the mRNA expresion levels of reactivity markers (Gfap,S10O),inflammatory factors( IL Iβ ,TNF-a,iNOS),Al-typeAs markers (Gbp2,H2–T23) ,and A2-type As markers (SIOOAIO,Ptx3) ,andWesternbloting wasused to measure thechangesintheprotein expresionlevelsofGFAPandiNOS.ResultsGinsenosideRglsignificantly reduced the mRNA expression levels of Gfap , SIOO ,iNOS, TNF–α ,and IL–Iβ ( F=11.09-136.70,q=6.43-16.01 , P<0.05 )and the protein expression levels of GFAP and iNOS in RAs (F=8.67,7.66,q=6.80,5.36,P<0.05) . Compared with the control group,the TGF- β1+Rg1 group had significant reductions in the A1-type markers Gb?2 and H2-T23( F=61.94 , 18.46,q=13.95,5.58,P<0.05) and significant increases in the A2-type markers S1ooA1o and Ptx3 ? ′F=25.46,31.11,q=7.70 , (204號(hào) 10.65,P<0.01) .Compared with the TGF- ?β1 group,the TGF group had significant reductions in the Al-type markers Gbp2 and H2 -T23 ?F=61.94,18.46,q=13.29,8.45,P<0.01) ,with no significant changes in A2-type markers(SlooA10, (20 Ptx3) .Conclusion Ginsenoside Rgl can inhibit TGF- ?β1 -induced reactive characteristics of As and promotes their phenotypic transformation from A1 phenotype to A2 phenotype.

[Key words]ginsenoside Rg1 ;astrocytes; transforming growth factor β1 ;phenotyp!

星形膠質(zhì)細(xì)胞(As)作為中樞神經(jīng)系統(tǒng)(CNS)中主要的神經(jīng)膠質(zhì)細(xì)胞,具有維持血腦屏障、突觸形成與傳遞等作用[1-6]。(剩余10596字)

目錄
monitor