目的探讨调脂对不同肥胖类型老年高血压患者降压疗效及动脉硬化的影响。方法从老年体检者中选择322例原发性高血压患者按照析因设计随机分为4组:调脂降压腹型肥胖组(A组)89例、调脂降压非腹型肥胖组(B组)75例、单纯降压腹型肥胖组(C组)8...目的探讨调脂对不同肥胖类型老年高血压患者降压疗效及动脉硬化的影响。方法从老年体检者中选择322例原发性高血压患者按照析因设计随机分为4组:调脂降压腹型肥胖组(A组)89例、调脂降压非腹型肥胖组(B组)75例、单纯降压腹型肥胖组(C组)87例、单纯降压非腹型肥胖组(D组)71例。各组均给予替米沙坦40mg/d,调脂降压治疗在此基础上给予瑞舒伐他汀10mg/d,为期6个月。结果 A、B、C和D组治疗后,收缩压、舒张压、体质量指数、腰围、TG、TC、空腹血糖、踝肱指数(ABI,0.90±0.15 vs 0.92±0.14 vs 0.85±0.14 vs 0.86±0.17)、心-踝血管指数(CAVI,7.62±0.73 vs 7.74±0.74 vs 8.11±0.76 vs 8.30±0.70)比较,差异均有统计学意义(P<0.05)。A、B、C和D组降压有效率比较,差异均有统计学意义(87.64%vs 92.00%vs 78.00%vs 83.10%,P<0.05)。CAVI与收缩压、脉压、TC、TG呈正相关(r=0.180,r=0.153,r=0.895,r=0.533,P<0.01),ABI与收缩压、舒张压呈正相关(r=0.415,r=0.123,P<0.05)。结论调脂对老年肥胖高血压患者降压疗效显著,有效改善动脉硬化症状,且无明显不良反应。展开更多
目的探讨小窝(caveolae)对雌激素通过G蛋白偶联雌激素受体(GPER)调控小鼠主动脉内皮型一氧化氮合酶(eNOS)活性的影响。方法当细胞融合度达到80%~90%时,选取内皮细胞分为对照1组、DMSO组、雌二醇1组、雌二醇2组、雌二醇3组(n=5),其中雌二...目的探讨小窝(caveolae)对雌激素通过G蛋白偶联雌激素受体(GPER)调控小鼠主动脉内皮型一氧化氮合酶(eNOS)活性的影响。方法当细胞融合度达到80%~90%时,选取内皮细胞分为对照1组、DMSO组、雌二醇1组、雌二醇2组、雌二醇3组(n=5),其中雌二醇1组、雌二醇2组、雌二醇3组按浓度梯度加入雌二醇(10、50、100 nmol/L),对照1组不予任何处理,DMSO组加入50μl DMSO培养。另选取内皮细胞分为对照2组(未作任何处理)、阴性对照1组[加入小窝蛋白1(Cav-1)阴性对照干扰RNA]、Cav-1敲减组(加入Cav-1干扰RNA);选取部分内皮细胞设对照3组(未作任何处理)、阴性对照2组(加入GPER阴性对照干扰RNA)、GPER敲减组(加入GPER干扰RNA)。检测Cav-1、GPER、eNOS、磷酸化eNOS(p-eNOS)蛋白表达。结果与对照1组比较,雌二醇3组p-eNOS蛋白表达明显增加(0.47±0.07 vs 0.20±0.04,P<0.05)。对照2组、阴性对照1组、Cav-1敲减组GPER、eNOS、Cav-1蛋白表达比较,差异有统计学意义(P<0.05,P<0.01)。与对照2组比较,Cav-1敲减组GPER、eNOS、Cav-1蛋白表达明显降低(P<0.05,P<0.01)。对照3组、阴性对照2组、GPER敲减组eNOS、p-eNOS表达比较,无统计学差异(P>0.05)。与对照3组比较,GPER敲减组GPER蛋白表达明显降低(0.56±0.22 vs 2.40±0.65,P<0.05)。结论小窝参与了雌激素通过GPER调控小鼠主动脉eNOS活性的过程。展开更多
Thromboangiitis obliterans(TAO)is a rare,chronic,progressive,and segmental inflammatory disease characterized by a high rate of amputation,significantly compromising the quality of life of patients.Si-Miao-Yong-An dec...Thromboangiitis obliterans(TAO)is a rare,chronic,progressive,and segmental inflammatory disease characterized by a high rate of amputation,significantly compromising the quality of life of patients.Si-Miao-Yong-An decoction(SMYA),a tradition-al prescription,exhibits anti-inflammatory,anti-thrombotic,and various other pharmacological properties.Clinically,it was fully proved to be effective for TAO therapy,but the specific therapeutic effect of SMYA on TAO has been unknown.Thus,deep unveiling the mechanism of SMYA in TAO for identifying clinical therapeutic targets is extremely important.In this study,we observed elev-ated levels of IL-17A in the peripheral blood mononuclear cells(PBMCs)of TAO patients,whereas the expression of miR-548j-5p was significantly decreased.A negative correlation between the levels of miR-548j-5p and IL-17A was also demonstrated.In vitro ex-periments showed that overexpression of miR-548j-5p led to a decrease in IL-17A levels,whereas downregulation of miR-548j-5p showed the opposite effect.Using a dual luciferase assay,we confirmed that miR-548j-5p directly targets IL-17A.Furthermore,serum containing SMYA effectively decreased IL-17A levels by increasing the expression of miR-548j-5p.More importantly,the results of in vivo tests indicated that SMYA mitigated the development of TAO by inhibiting IL-17A through the upregulation of miR-548j-5p in vascular tissues.In conclusion,SMYA significantly enhances the expression of miR-548j-5p,thereby reducing the levels of the target gene IL-17A and alleviating TAO.Our research not only identifies novel targets and pathways for the clinical diagnosis and treatment of TAO but also advances the innovation in traditional Chinese medicine through the elucidation of the SMYA/miR-548j-5p/IL-17A regulatory axis in the pathogenesis of TAO.展开更多
文摘目的探讨调脂对不同肥胖类型老年高血压患者降压疗效及动脉硬化的影响。方法从老年体检者中选择322例原发性高血压患者按照析因设计随机分为4组:调脂降压腹型肥胖组(A组)89例、调脂降压非腹型肥胖组(B组)75例、单纯降压腹型肥胖组(C组)87例、单纯降压非腹型肥胖组(D组)71例。各组均给予替米沙坦40mg/d,调脂降压治疗在此基础上给予瑞舒伐他汀10mg/d,为期6个月。结果 A、B、C和D组治疗后,收缩压、舒张压、体质量指数、腰围、TG、TC、空腹血糖、踝肱指数(ABI,0.90±0.15 vs 0.92±0.14 vs 0.85±0.14 vs 0.86±0.17)、心-踝血管指数(CAVI,7.62±0.73 vs 7.74±0.74 vs 8.11±0.76 vs 8.30±0.70)比较,差异均有统计学意义(P<0.05)。A、B、C和D组降压有效率比较,差异均有统计学意义(87.64%vs 92.00%vs 78.00%vs 83.10%,P<0.05)。CAVI与收缩压、脉压、TC、TG呈正相关(r=0.180,r=0.153,r=0.895,r=0.533,P<0.01),ABI与收缩压、舒张压呈正相关(r=0.415,r=0.123,P<0.05)。结论调脂对老年肥胖高血压患者降压疗效显著,有效改善动脉硬化症状,且无明显不良反应。
文摘目的探讨小窝(caveolae)对雌激素通过G蛋白偶联雌激素受体(GPER)调控小鼠主动脉内皮型一氧化氮合酶(eNOS)活性的影响。方法当细胞融合度达到80%~90%时,选取内皮细胞分为对照1组、DMSO组、雌二醇1组、雌二醇2组、雌二醇3组(n=5),其中雌二醇1组、雌二醇2组、雌二醇3组按浓度梯度加入雌二醇(10、50、100 nmol/L),对照1组不予任何处理,DMSO组加入50μl DMSO培养。另选取内皮细胞分为对照2组(未作任何处理)、阴性对照1组[加入小窝蛋白1(Cav-1)阴性对照干扰RNA]、Cav-1敲减组(加入Cav-1干扰RNA);选取部分内皮细胞设对照3组(未作任何处理)、阴性对照2组(加入GPER阴性对照干扰RNA)、GPER敲减组(加入GPER干扰RNA)。检测Cav-1、GPER、eNOS、磷酸化eNOS(p-eNOS)蛋白表达。结果与对照1组比较,雌二醇3组p-eNOS蛋白表达明显增加(0.47±0.07 vs 0.20±0.04,P<0.05)。对照2组、阴性对照1组、Cav-1敲减组GPER、eNOS、Cav-1蛋白表达比较,差异有统计学意义(P<0.05,P<0.01)。与对照2组比较,Cav-1敲减组GPER、eNOS、Cav-1蛋白表达明显降低(P<0.05,P<0.01)。对照3组、阴性对照2组、GPER敲减组eNOS、p-eNOS表达比较,无统计学差异(P>0.05)。与对照3组比较,GPER敲减组GPER蛋白表达明显降低(0.56±0.22 vs 2.40±0.65,P<0.05)。结论小窝参与了雌激素通过GPER调控小鼠主动脉eNOS活性的过程。
基金supported by the Natural Sci-ence Foundation of China(No.82274575)Co-construction Project of State Administration of TCM(Nos.GZY-KJS-SD-2023-034,GZY-KJS-SD-2023-046)+4 种基金Major Basic Research Project of Natural Science Foundation of Shandong Province(No.ZR2023ZD56)the Joint Fund of Natural Science Foundation of Shandong(No.ZR2022LZY011)the Central Government Guides Local Science and Technology Development Fund Projects of Shandong Province(No.YDZX20203700001407)Taishan Scholars(No.Tsqn201812125)National Youth Qihuang Scholar Training Program,Shandong Province Traditional Chinese Medicine High Level Talent Cultivation Project and Key research and development project of Shandong Province(No.2020CXGC010505).
文摘Thromboangiitis obliterans(TAO)is a rare,chronic,progressive,and segmental inflammatory disease characterized by a high rate of amputation,significantly compromising the quality of life of patients.Si-Miao-Yong-An decoction(SMYA),a tradition-al prescription,exhibits anti-inflammatory,anti-thrombotic,and various other pharmacological properties.Clinically,it was fully proved to be effective for TAO therapy,but the specific therapeutic effect of SMYA on TAO has been unknown.Thus,deep unveiling the mechanism of SMYA in TAO for identifying clinical therapeutic targets is extremely important.In this study,we observed elev-ated levels of IL-17A in the peripheral blood mononuclear cells(PBMCs)of TAO patients,whereas the expression of miR-548j-5p was significantly decreased.A negative correlation between the levels of miR-548j-5p and IL-17A was also demonstrated.In vitro ex-periments showed that overexpression of miR-548j-5p led to a decrease in IL-17A levels,whereas downregulation of miR-548j-5p showed the opposite effect.Using a dual luciferase assay,we confirmed that miR-548j-5p directly targets IL-17A.Furthermore,serum containing SMYA effectively decreased IL-17A levels by increasing the expression of miR-548j-5p.More importantly,the results of in vivo tests indicated that SMYA mitigated the development of TAO by inhibiting IL-17A through the upregulation of miR-548j-5p in vascular tissues.In conclusion,SMYA significantly enhances the expression of miR-548j-5p,thereby reducing the levels of the target gene IL-17A and alleviating TAO.Our research not only identifies novel targets and pathways for the clinical diagnosis and treatment of TAO but also advances the innovation in traditional Chinese medicine through the elucidation of the SMYA/miR-548j-5p/IL-17A regulatory axis in the pathogenesis of TAO.
