Scutellarin(SCU), a flavonoid from a traditional Chinese medicinal plant. Our previous study has demonstrated that SCU relaxes mouse aortic arteries mainly in an endothelium-depend-ent manner. In the present study, we...Scutellarin(SCU), a flavonoid from a traditional Chinese medicinal plant. Our previous study has demonstrated that SCU relaxes mouse aortic arteries mainly in an endothelium-depend-ent manner. In the present study, we investigated the vasoprotective effects of SCU against HR-induced endothelial dysfunction(ED) in isolated rat CA and the possible mechanisms involving cyclic guanosine monophosphate(c GMP) dependent protein kinase(PKG). The isolated endothelium-intact and endothelium-denuded rat CA rings were treated with HR injury. Evaluation of endothelium-dependent and-independent vasodilation relaxation of the CA rings were performed using wire myography and the protein expressions were assayed by Western blotting. SCU(10–1 000 μmol·L-1) could relax the endothelium-intact CA rings but not endothelium-denuded ones. In the intact CA rings, the PKG inhibitor, Rp-8-Br-c GMPS(PKGI-rp, 4 μmol·L-1), significantly blocked SCU(10–1 000 μmol·L-1)-induced relaxation. The NO synthase(NOS) inhibitor, NO-nitro-L-arginine methylester(L-NAME, 100 μmol·L-1), did not significantly change the effects of SCU(10–1 000 μmol·L-1). HR treatment significantly impaired ACh-induced relaxation, which was reversed by pre-incubation with SCU(500 μmol·L-1), while HR treatment did not altered NTG-induced vasodilation. PKGI-rp(4 μmol·L-1) blocked the protective effects of SCU in HR-treated CA rings. Additionally, HR treatment reduced phosphorylated vasodilator-stimulated phosphoprotein(p-VASP,phosphorylated product of PKG), which was reversed by SCU pre-incubation, suggesting that SCU activated PKG phosphorylation against HR injury. SCU induces CA vasodilation in an endothelium-dependent manner to and repairs HR-induced impairment via activation of PKG signaling pathway.展开更多
OBJECTIVE:To investigate the efficacy of Gouqizi(Fructus Lycii)seed oil(FLSO)on D-gal induced inflammation in testis of rats in vitro and in vivo.METHODS:In aging Sertoli cells(TM4 cells)induced by D-galactose(D-gal),...OBJECTIVE:To investigate the efficacy of Gouqizi(Fructus Lycii)seed oil(FLSO)on D-gal induced inflammation in testis of rats in vitro and in vivo.METHODS:In aging Sertoli cells(TM4 cells)induced by D-galactose(D-gal),the expression of upregulated agingrelated proteins.The number of cells counted by cell counting kit(CCK)-8 assay showed a high number of cells disposed with FLSO at 50,100 and 150μg/mL compared to that for the aging model.In vivo,male Sprague–Dawley rats(n=50,8-week-old,230-255 g)were randomly categorized into control,aging model,and FLSO(low-,medium-,and high-dose)groups.The expression of nuclear factor-κB(NF-κB)and its upstream factors[Janus kinase 1(JAK1)and signal transducerand activator of transcription 1(STAT1)]was detected by Western blot and immunofluorescence,related inflammatory factors quantified by enzyme-linked immunosorbent assay.Evaluation of testicular tissue by Johnsen score,the spermatogenic function was explored.RESULTS:The expression of interleukin-1β(IL-1β)(P<0.05),IL-6(P<0.001),and tumor necrosis factorα(TNF-α)(P<0.05)was decreased significantly,while that of heme oxygenase-1(HO-1)(P<0.001)and IL-10(P<0.05)was increased in cells disposed with FLSO 100μg/mL.FLSO inhibited the expression of NF-κB and declined pp65/p65(P<0.01),as detected by Western blotting.In vivo,the levels in serum of IL-1β(P<0.001),IL-6(P<0.05),and TNF-α(P<0.01)declined while IL-10(P<0.05)was upregulated post-FLSO treatment.In addition,the expression of JAK-1 and STAT1 increased significantly in testicular tissue of rats treated with FLSO as compared to the aging model of rats(P<0.001),while the expression of NF-κB(P<0.001)declined in the testis in the FLSO group,as assessed by immunofluorescence.The levels of inhibor B and testosterone in serum both increased(P<0.05).CONCLUSIONS:In conclusion,this study determined the protective effects of FLSO to tolerate inflammatory injury in the testis,indicating that FLSO alleviates inflammation via JAK-1/STAT1/NF-κB pathway.展开更多
目的检测多囊卵巢综合征(PCOS)合并代谢综合征(MS)患者血清miR-222-3p的表达水平,分析其与糖脂代谢指标的相关性。方法选取西安国际医学中心医院2020年1月至2021年12月收治的160例PCOS患者作为研究对象,根据是否合并MS分为单纯PCOS组(10...目的检测多囊卵巢综合征(PCOS)合并代谢综合征(MS)患者血清miR-222-3p的表达水平,分析其与糖脂代谢指标的相关性。方法选取西安国际医学中心医院2020年1月至2021年12月收治的160例PCOS患者作为研究对象,根据是否合并MS分为单纯PCOS组(105例)和PCOS+MS组(55例),比较2组空腹胰岛素(FINS)、空腹血糖(FPG)、餐后2 h血糖(2 h PG)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)水平,计算胰岛素抵抗指数(HOMA-IR)。采用滚环扩增(RCA)技术检测2组患者血清miR-222-3p表达水平。采用Pearson相关分析miR-222-3p表达水平与糖脂代谢指标的相关性。采用受试者工作特征(ROC)曲线分析miR-222-3p诊断PCOS患者发生MS的价值。结果PCOS+MS组血清FPG、2 h PG、FINS、TC、TG、LDL-C水平及HOMA-IR明显高于单纯PCOS组(P<0.05),HDL-C水平明显低于单纯PCOS组(P<0.05)。与单纯PCOS组比较,PCOS+MS组血清miR-222-3p表达水平明显升高(P<0.05)。PCOS患者miR-222-3p表达水平与FPG、2 h PG、FINS、HOMA-IR、TC、TG、LDL-C均呈正相关(P<0.05),与HDL-C呈负相关(P<0.05)。ROC曲线分析结果显示,miR-222-3p诊断PCOS发生MS的曲线下面积为0.806(95%CI:0.729~0.883),当截断值为2.32时,约登指数最大(0.526),此时的灵敏度为87.62%,特异度为65.00%。结论miR-222-3p在PCOS合并MS患者中表达水平较高,且与患者糖脂代谢紊乱密切相关。展开更多
基金supported by the National Natural Science Foundation of China(Nos.30960450,81173110)Yunnan Provincial Science and Technology Department(Nos.2011FA 022,2012BC012,2014FA010,2014FB037,2014BC012)
文摘Scutellarin(SCU), a flavonoid from a traditional Chinese medicinal plant. Our previous study has demonstrated that SCU relaxes mouse aortic arteries mainly in an endothelium-depend-ent manner. In the present study, we investigated the vasoprotective effects of SCU against HR-induced endothelial dysfunction(ED) in isolated rat CA and the possible mechanisms involving cyclic guanosine monophosphate(c GMP) dependent protein kinase(PKG). The isolated endothelium-intact and endothelium-denuded rat CA rings were treated with HR injury. Evaluation of endothelium-dependent and-independent vasodilation relaxation of the CA rings were performed using wire myography and the protein expressions were assayed by Western blotting. SCU(10–1 000 μmol·L-1) could relax the endothelium-intact CA rings but not endothelium-denuded ones. In the intact CA rings, the PKG inhibitor, Rp-8-Br-c GMPS(PKGI-rp, 4 μmol·L-1), significantly blocked SCU(10–1 000 μmol·L-1)-induced relaxation. The NO synthase(NOS) inhibitor, NO-nitro-L-arginine methylester(L-NAME, 100 μmol·L-1), did not significantly change the effects of SCU(10–1 000 μmol·L-1). HR treatment significantly impaired ACh-induced relaxation, which was reversed by pre-incubation with SCU(500 μmol·L-1), while HR treatment did not altered NTG-induced vasodilation. PKGI-rp(4 μmol·L-1) blocked the protective effects of SCU in HR-treated CA rings. Additionally, HR treatment reduced phosphorylated vasodilator-stimulated phosphoprotein(p-VASP,phosphorylated product of PKG), which was reversed by SCU pre-incubation, suggesting that SCU activated PKG phosphorylation against HR injury. SCU induces CA vasodilation in an endothelium-dependent manner to and repairs HR-induced impairment via activation of PKG signaling pathway.
基金Supported by Natural Science Foundation-funded Project:Activation of SIRT3 by Gouqizi(Fructus Lycii)Seed Oil to Improve Mitochondrial Function and Maintain Homeostasis in Injured Testis of Sub-acutely Aging Male Rats(No.81860876)Ningxia Natural Science Foundation-funded Project:Effects of Active Components of Gouqizi(Fructus Lycii)Seed Oil on Regulating Autophagy and Inflammation and Delaying Testicular Aging in Sub-acutely Aging Male Rats(No.2020AAC02016)。
文摘OBJECTIVE:To investigate the efficacy of Gouqizi(Fructus Lycii)seed oil(FLSO)on D-gal induced inflammation in testis of rats in vitro and in vivo.METHODS:In aging Sertoli cells(TM4 cells)induced by D-galactose(D-gal),the expression of upregulated agingrelated proteins.The number of cells counted by cell counting kit(CCK)-8 assay showed a high number of cells disposed with FLSO at 50,100 and 150μg/mL compared to that for the aging model.In vivo,male Sprague–Dawley rats(n=50,8-week-old,230-255 g)were randomly categorized into control,aging model,and FLSO(low-,medium-,and high-dose)groups.The expression of nuclear factor-κB(NF-κB)and its upstream factors[Janus kinase 1(JAK1)and signal transducerand activator of transcription 1(STAT1)]was detected by Western blot and immunofluorescence,related inflammatory factors quantified by enzyme-linked immunosorbent assay.Evaluation of testicular tissue by Johnsen score,the spermatogenic function was explored.RESULTS:The expression of interleukin-1β(IL-1β)(P<0.05),IL-6(P<0.001),and tumor necrosis factorα(TNF-α)(P<0.05)was decreased significantly,while that of heme oxygenase-1(HO-1)(P<0.001)and IL-10(P<0.05)was increased in cells disposed with FLSO 100μg/mL.FLSO inhibited the expression of NF-κB and declined pp65/p65(P<0.01),as detected by Western blotting.In vivo,the levels in serum of IL-1β(P<0.001),IL-6(P<0.05),and TNF-α(P<0.01)declined while IL-10(P<0.05)was upregulated post-FLSO treatment.In addition,the expression of JAK-1 and STAT1 increased significantly in testicular tissue of rats treated with FLSO as compared to the aging model of rats(P<0.001),while the expression of NF-κB(P<0.001)declined in the testis in the FLSO group,as assessed by immunofluorescence.The levels of inhibor B and testosterone in serum both increased(P<0.05).CONCLUSIONS:In conclusion,this study determined the protective effects of FLSO to tolerate inflammatory injury in the testis,indicating that FLSO alleviates inflammation via JAK-1/STAT1/NF-κB pathway.
文摘目的检测多囊卵巢综合征(PCOS)合并代谢综合征(MS)患者血清miR-222-3p的表达水平,分析其与糖脂代谢指标的相关性。方法选取西安国际医学中心医院2020年1月至2021年12月收治的160例PCOS患者作为研究对象,根据是否合并MS分为单纯PCOS组(105例)和PCOS+MS组(55例),比较2组空腹胰岛素(FINS)、空腹血糖(FPG)、餐后2 h血糖(2 h PG)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)水平,计算胰岛素抵抗指数(HOMA-IR)。采用滚环扩增(RCA)技术检测2组患者血清miR-222-3p表达水平。采用Pearson相关分析miR-222-3p表达水平与糖脂代谢指标的相关性。采用受试者工作特征(ROC)曲线分析miR-222-3p诊断PCOS患者发生MS的价值。结果PCOS+MS组血清FPG、2 h PG、FINS、TC、TG、LDL-C水平及HOMA-IR明显高于单纯PCOS组(P<0.05),HDL-C水平明显低于单纯PCOS组(P<0.05)。与单纯PCOS组比较,PCOS+MS组血清miR-222-3p表达水平明显升高(P<0.05)。PCOS患者miR-222-3p表达水平与FPG、2 h PG、FINS、HOMA-IR、TC、TG、LDL-C均呈正相关(P<0.05),与HDL-C呈负相关(P<0.05)。ROC曲线分析结果显示,miR-222-3p诊断PCOS发生MS的曲线下面积为0.806(95%CI:0.729~0.883),当截断值为2.32时,约登指数最大(0.526),此时的灵敏度为87.62%,特异度为65.00%。结论miR-222-3p在PCOS合并MS患者中表达水平较高,且与患者糖脂代谢紊乱密切相关。
