目的比较达格列净和利格列汀用于治疗超重或肥胖2型糖尿病(T2DM)伴微量白蛋白尿患者的临床效果。方法选取2019年4月—2020年4月在广东省佛山市南海区第七人民医院诊断为超重或肥胖T2DM伴微量白蛋白尿的58例患者作为研究对象,按照随机数...目的比较达格列净和利格列汀用于治疗超重或肥胖2型糖尿病(T2DM)伴微量白蛋白尿患者的临床效果。方法选取2019年4月—2020年4月在广东省佛山市南海区第七人民医院诊断为超重或肥胖T2DM伴微量白蛋白尿的58例患者作为研究对象,按照随机数字表法将其分为达格列净组和利格列汀组,每组各29例。两组患者均使用二甲双胍进行基础治疗。比较两组患者的血糖相关指标、胰岛素抵抗指数、肾功能相关指标及不良反应。结果治疗后,两组患者的空腹血糖(FPG)、餐后2 h血糖(2 h PG)、糖化血红蛋白(GHb)均低于治疗前,且达格列净组患者的FPG、2 h PG、GHb均低于利格列汀组,差异有统计学意义(P<0.05)。治疗后,两组患者的胰岛素抵抗指数低于治疗前,且达格列净组患者的胰岛素抵抗指数低于利格列汀组,差异有统计学意义(P<0.05)。治疗后,两组患者的尿微量白蛋白(UAlb)、尿白蛋白/肌酐比值(UACR)、血清肌酐浓度(SCr)均低于治疗前,且达格列净组患者的UAlb、UACR、SCr均低于利格列汀组,差异有统计学意义(P<0.05)。两组患者的不良反应总发生率比较,差异无统计学意义(P>0.05)。结论达格列净可有效改善超重或肥胖T2DM伴微白蛋白尿患者的血糖,降低胰岛素抵抗指数,改善肾功能,降低不良反应发生率。展开更多
Macrophages play an important role in inflammation, and excessive and chronic activation of macrophages leads to systemic inflammatory diseases, such as atherosclerosis and rheumatoid arthritis. In this paper, we expl...Macrophages play an important role in inflammation, and excessive and chronic activation of macrophages leads to systemic inflammatory diseases, such as atherosclerosis and rheumatoid arthritis. In this paper, we explored the anti-inflammatory effect of broussonin E, a novel phenolic compound isolated from the barks of Broussonetia kanzinoki, and its underlying molecular mechanisms. We discovered that Broussonin E could suppress the LPS-induced pro-inflammatory production in RAW264.7 cells, involving TNF-α, IL-1β, IL-6, COX-2 and iNOS. And broussonin E enhanced the expressions of anti-inflammatory mediators such as IL-10, CD206 and arginase-1(Arg-1) in LPS-stimulated RAW264.7 cells. Further, we demonstrated that broussonin E inhibited the LPS-stimulated phosphorylation of ERK and p38 MAPK. Moreover, we found that broussonin E could activate janus kinase(JAK) 2, signal transducer and activator of transcription(STAT) 3. Downregulated pro-inflammatory cytokines and upregulated anti-inflammatory factors by broussonin E were abolished by using the inhibitor of JAK2-STAT3 pathway, WP1066. Taken together, our results showed that broussonin E could suppress inflammation by modulating macrophages activation state via inhibiting the ERK and p38 MAPK and enhancing JAK2-STAT3 signaling pathway, and can be further developed as a promising drug for the treatment of inflammation-related diseases such as atherosclerosis.展开更多
文摘目的比较达格列净和利格列汀用于治疗超重或肥胖2型糖尿病(T2DM)伴微量白蛋白尿患者的临床效果。方法选取2019年4月—2020年4月在广东省佛山市南海区第七人民医院诊断为超重或肥胖T2DM伴微量白蛋白尿的58例患者作为研究对象,按照随机数字表法将其分为达格列净组和利格列汀组,每组各29例。两组患者均使用二甲双胍进行基础治疗。比较两组患者的血糖相关指标、胰岛素抵抗指数、肾功能相关指标及不良反应。结果治疗后,两组患者的空腹血糖(FPG)、餐后2 h血糖(2 h PG)、糖化血红蛋白(GHb)均低于治疗前,且达格列净组患者的FPG、2 h PG、GHb均低于利格列汀组,差异有统计学意义(P<0.05)。治疗后,两组患者的胰岛素抵抗指数低于治疗前,且达格列净组患者的胰岛素抵抗指数低于利格列汀组,差异有统计学意义(P<0.05)。治疗后,两组患者的尿微量白蛋白(UAlb)、尿白蛋白/肌酐比值(UACR)、血清肌酐浓度(SCr)均低于治疗前,且达格列净组患者的UAlb、UACR、SCr均低于利格列汀组,差异有统计学意义(P<0.05)。两组患者的不良反应总发生率比较,差异无统计学意义(P>0.05)。结论达格列净可有效改善超重或肥胖T2DM伴微白蛋白尿患者的血糖,降低胰岛素抵抗指数,改善肾功能,降低不良反应发生率。
基金supported by the National Natural Science Foundation of China(Nos.81703530 and 81773995)the Natural Science Foundation of Jiangsu Province(Nos.BK20160032 and BK20170859)+2 种基金the Opening Project of Zhejiang Provincial Preponderant and Characteristic Subject of Key University(Traditional Chinese Pharmacology)Zhejiang Chinese Medical University(No.ZYAOX2018001)the Six Talent Peaks Project of Jiangsu Province(PANG Tao)
文摘Macrophages play an important role in inflammation, and excessive and chronic activation of macrophages leads to systemic inflammatory diseases, such as atherosclerosis and rheumatoid arthritis. In this paper, we explored the anti-inflammatory effect of broussonin E, a novel phenolic compound isolated from the barks of Broussonetia kanzinoki, and its underlying molecular mechanisms. We discovered that Broussonin E could suppress the LPS-induced pro-inflammatory production in RAW264.7 cells, involving TNF-α, IL-1β, IL-6, COX-2 and iNOS. And broussonin E enhanced the expressions of anti-inflammatory mediators such as IL-10, CD206 and arginase-1(Arg-1) in LPS-stimulated RAW264.7 cells. Further, we demonstrated that broussonin E inhibited the LPS-stimulated phosphorylation of ERK and p38 MAPK. Moreover, we found that broussonin E could activate janus kinase(JAK) 2, signal transducer and activator of transcription(STAT) 3. Downregulated pro-inflammatory cytokines and upregulated anti-inflammatory factors by broussonin E were abolished by using the inhibitor of JAK2-STAT3 pathway, WP1066. Taken together, our results showed that broussonin E could suppress inflammation by modulating macrophages activation state via inhibiting the ERK and p38 MAPK and enhancing JAK2-STAT3 signaling pathway, and can be further developed as a promising drug for the treatment of inflammation-related diseases such as atherosclerosis.
