目的探讨益肾通络解毒汤对气阴两虚兼毒瘀互结型糖尿病肾病的临床疗效及对氧化应激的影响。方法选取2018年1月—2019年6月医院收治的120例气阴两虚兼毒瘀互结型糖尿病肾病患者,随后依据患者就诊顺序将其分为观察组及对照组各60例,两组...目的探讨益肾通络解毒汤对气阴两虚兼毒瘀互结型糖尿病肾病的临床疗效及对氧化应激的影响。方法选取2018年1月—2019年6月医院收治的120例气阴两虚兼毒瘀互结型糖尿病肾病患者,随后依据患者就诊顺序将其分为观察组及对照组各60例,两组均予以口服降糖药、皮注胰岛素、运动疗法、饮食控制等基础治疗,在基础治疗上对照组加以尿毒清颗粒治疗,观察组予以益肾通络解毒汤治疗,比较治疗前后两组肾脏功能指标[肾小球滤过率(eGFR)、血肌酐(SCr)、24 h尿蛋白排泄率(24 h UAER)]、炎症指标[白细胞介素-6(IL-6)、超敏C反应蛋白(hsCRP)]、氧化应激指标[8-羟基脱氧鸟嘌呤(8-OHdG)、晚期糖基化终产物(AGEs)、丙二醛(MDA)、活性氧(ROS)、超氧化物歧化酶(SOD)、晚期氧化蛋白产物(AOPP)]变化情况,并比较两组病人的临床疗效。结果两组治疗疗程结束后,观察组肾功能、炎症反应及氧化应激水平各项指标均明显优于对照组(P<0.05)。观察组总有效率为90.00%,对照组总有效率为70.00%,观察组优于对照组(P<0.05)。结论益肾通络解毒汤治疗气阴两虚兼毒瘀互结型糖尿病肾病患者疗效确切,能有效改善患者的肾功能,其机制可能与其抑制炎症反应及抗氧化应激相关。展开更多
This study aimed to investigate whether pitavastatin protected against injury induced by advanced glycation end products products（AGEs） in neonatal rat cardiomyocytes,and to examine the underlying mechanisms.Cardiom...This study aimed to investigate whether pitavastatin protected against injury induced by advanced glycation end products products（AGEs） in neonatal rat cardiomyocytes,and to examine the underlying mechanisms.Cardiomyocytes of neonatal rats were incubated for 48 hours with AGEs（100 μg/mL）,receptor for advanced glycation end products（RAGE）,antibody（1 μg/mL） and pitavastatin（600 ng/mL）.The levels of p62 and beclinl were determined by Western blotting.Mitochondrial membrane potential（△Ψm） and the generation of reactive oxygen species（ROS） were measured through the JC-1 and DCFH-DA.In the AGEs group,the expression of beclinl was remarkably increased compared to the control group,while the expression of p62 was significantly decreased.AGEs also markedly decreased △Ψm and significantly increased ROS compared with the control group.After treatment with RAGE antibody or pitavastatin,the level of beclinl was markedly decreased compared with the AGEs group,but the level of p62 was remarkably increased.In the AGEs ＋ RAGE antibody group and AGEs＋ pitavastatin group,△Ψm was significantly increased and ROS was remarkably decreased compared with the AGEs group.In conclusion,AGEs-RAGE may induce autophagy of cardiomyocytes by generation of ROS and pitavastatin could protect against AGEs-induced injury against cardiomyocytes.展开更多
Qifu-Yin(QFY), a widely used formula of traditional Chinese medicine(TCM) derived from "Jingyue Quanshu", is one of the most commonly used TCM prescriptions for the clinical treatment of Alzheimer disease. T...Qifu-Yin(QFY), a widely used formula of traditional Chinese medicine(TCM) derived from "Jingyue Quanshu", is one of the most commonly used TCM prescriptions for the clinical treatment of Alzheimer disease. The role of advanced glycation end products(AGEs) and its receptor RAGE have attracted increasing attention as the pivotal role of Aβ has been questioned. The present study was designed to test the neuroprotective effects of QFY, and the possible mechanism in AGE-induced Alzheimer model rats. After injection of AGE in the CA3 area of the hippocampus, QFY(8.6, 4.3, and 2.15 g·kg–1), and a positive control drug donepezil(2 mg·kg–1) were administrated through gastric intubation to rats once daily for thirty consecutive days. Another positive control group was the AGE + anti-RAGE group, which was simultaneously injected with anti-RAGE antibody before AGE treatment. The control group, sham-operated group, as well as the AGE + anti-RAGE group received saline at the same dosage. The Morris water maze test and the step-down passive avoidance test were conducted to evaluate the cognitive function of the rats. The expression of RAGE and NF-κB were assayed by immunohistochemical staining. The levels of Aβ, TNF-α, and IL-1β in the hippocampus were measured by enzyme-linked immunosorbent assay(ELISA). The results showed that QFY could significantly attenuate the memory impairment induced by AGE, decrease the expressions of RAGE and NF-κB, and reduce the levels of Aβ, TNF-α, and IL-1β in the hippocampus in a dose-dependent manner. Also, the blockage of RAGE could significantly reduce the impairments caused by AGEs. In conclusion, QFY could attenuate AGEs-induced, Alzheimer-like pathophysiological changes. These neuroprotective effects might be related to the RAGE/NF-κB pathway and its anti-inflammatory activity.展开更多
文摘目的探讨益肾通络解毒汤对气阴两虚兼毒瘀互结型糖尿病肾病的临床疗效及对氧化应激的影响。方法选取2018年1月—2019年6月医院收治的120例气阴两虚兼毒瘀互结型糖尿病肾病患者,随后依据患者就诊顺序将其分为观察组及对照组各60例,两组均予以口服降糖药、皮注胰岛素、运动疗法、饮食控制等基础治疗,在基础治疗上对照组加以尿毒清颗粒治疗,观察组予以益肾通络解毒汤治疗,比较治疗前后两组肾脏功能指标[肾小球滤过率(eGFR)、血肌酐(SCr)、24 h尿蛋白排泄率(24 h UAER)]、炎症指标[白细胞介素-6(IL-6)、超敏C反应蛋白(hsCRP)]、氧化应激指标[8-羟基脱氧鸟嘌呤(8-OHdG)、晚期糖基化终产物(AGEs)、丙二醛(MDA)、活性氧(ROS)、超氧化物歧化酶(SOD)、晚期氧化蛋白产物(AOPP)]变化情况,并比较两组病人的临床疗效。结果两组治疗疗程结束后,观察组肾功能、炎症反应及氧化应激水平各项指标均明显优于对照组(P<0.05)。观察组总有效率为90.00%,对照组总有效率为70.00%,观察组优于对照组(P<0.05)。结论益肾通络解毒汤治疗气阴两虚兼毒瘀互结型糖尿病肾病患者疗效确切,能有效改善患者的肾功能,其机制可能与其抑制炎症反应及抗氧化应激相关。
基金supported by the National NaturalScience Foundation of China(NSFC 81570328,Wang Junhong)the"Sixth-Peak Talent"of Jiangsu Province(2011WSN-029 to Prof.Guo Yan and2013WSN-036 to Dr.Wang Junhong)support by the Health Department of Jiangsu Province(z201301)
文摘This study aimed to investigate whether pitavastatin protected against injury induced by advanced glycation end products products（AGEs） in neonatal rat cardiomyocytes,and to examine the underlying mechanisms.Cardiomyocytes of neonatal rats were incubated for 48 hours with AGEs（100 μg/mL）,receptor for advanced glycation end products（RAGE）,antibody（1 μg/mL） and pitavastatin（600 ng/mL）.The levels of p62 and beclinl were determined by Western blotting.Mitochondrial membrane potential（△Ψm） and the generation of reactive oxygen species（ROS） were measured through the JC-1 and DCFH-DA.In the AGEs group,the expression of beclinl was remarkably increased compared to the control group,while the expression of p62 was significantly decreased.AGEs also markedly decreased △Ψm and significantly increased ROS compared with the control group.After treatment with RAGE antibody or pitavastatin,the level of beclinl was markedly decreased compared with the AGEs group,but the level of p62 was remarkably increased.In the AGEs ＋ RAGE antibody group and AGEs＋ pitavastatin group,△Ψm was significantly increased and ROS was remarkably decreased compared with the AGEs group.In conclusion,AGEs-RAGE may induce autophagy of cardiomyocytes by generation of ROS and pitavastatin could protect against AGEs-induced injury against cardiomyocytes.
基金supported by the Scientific Research Project of Administration of Traditional Medicine of Shanxi Province(13-ZY017)the Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)+2 种基金supported by grants from the Natural Science Foundation of Jiangsu Province of China(Grant No.BK2011630)the Fundamental Research Funds for the Central Universities(Program No.JKQ2011036)the Research Innovation Program Project for Graduate Students in Jiangsu Province(CXZZ13_03)
文摘Qifu-Yin(QFY), a widely used formula of traditional Chinese medicine(TCM) derived from "Jingyue Quanshu", is one of the most commonly used TCM prescriptions for the clinical treatment of Alzheimer disease. The role of advanced glycation end products(AGEs) and its receptor RAGE have attracted increasing attention as the pivotal role of Aβ has been questioned. The present study was designed to test the neuroprotective effects of QFY, and the possible mechanism in AGE-induced Alzheimer model rats. After injection of AGE in the CA3 area of the hippocampus, QFY(8.6, 4.3, and 2.15 g·kg–1), and a positive control drug donepezil(2 mg·kg–1) were administrated through gastric intubation to rats once daily for thirty consecutive days. Another positive control group was the AGE + anti-RAGE group, which was simultaneously injected with anti-RAGE antibody before AGE treatment. The control group, sham-operated group, as well as the AGE + anti-RAGE group received saline at the same dosage. The Morris water maze test and the step-down passive avoidance test were conducted to evaluate the cognitive function of the rats. The expression of RAGE and NF-κB were assayed by immunohistochemical staining. The levels of Aβ, TNF-α, and IL-1β in the hippocampus were measured by enzyme-linked immunosorbent assay(ELISA). The results showed that QFY could significantly attenuate the memory impairment induced by AGE, decrease the expressions of RAGE and NF-κB, and reduce the levels of Aβ, TNF-α, and IL-1β in the hippocampus in a dose-dependent manner. Also, the blockage of RAGE could significantly reduce the impairments caused by AGEs. In conclusion, QFY could attenuate AGEs-induced, Alzheimer-like pathophysiological changes. These neuroprotective effects might be related to the RAGE/NF-κB pathway and its anti-inflammatory activity.
