机构地区:[1]Department of Traditional Chinese Medicine,Suzhou Xiangcheng People's Hospital,Suzhou 215100,Jiangsu Province,China [2]Key Laboratory of Acupuncture and Medicine Research of Ministry of Education,Nanjing University of Chinese Medicine,Nanjing 210023,Jiangsu Province,China [3]College of Traditional Chinese Medicine,Jiangsu Vocational College of Medicine,Yancheng 224000,Jiangsu Province,China
出 处:《World Journal of Diabetes》2025年第2期133-150,共18页世界糖尿病杂志(英文)
基 金:National Natural Science Foundation of China,No.82074532,No.82374577,No.82305375,No.82305376,and No.82405567;The Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD).
摘 要:BACKGROUND Peripheral neuropathy caused by diabetes is closely related to the vicious cycle of oxidative stress and mitochondrial dysfunction resulting from metabolic abnormalities.The effects mediated by the silent information regulator type 2 homolog-1(SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator-1α(PGC-1α)axis present new opportunities for the treatment of type 2 diabetic peripheral neuropathy(T2DPN),potentially breaking this harmful cycle.AIM To validate the effectiveness of electroacupuncture(EA)in the treatment of T2DPN and investigate its potential mechanism based on the SIRT1/PGC-1αaxis.METHODS The effects of EA were evaluated through assessments of metabolic changes,morphological observations,and functional examinations of the sciatic nerve,along with measurements of inflammation and oxidative stress.Proteins related to the SIRT1/PGC-1αaxis,involved in the regulation of mitochondrial biogenesis and antioxidative stress,were detected in the sciatic nerve using Western blotting to explain the underlying mechanism.A counterevidence group was created by injecting a SIRT1 inhibitor during EA intervention to support the hypothesis.RESULTS In addition to diabetes-related metabolic changes,T2DPN rats showed significant reductions in pain threshold after 9 weeks,suggesting abnormal peripheral nerve function.EA treatment partially restored metabolic control and reduced nerve damage in T2DPN rats.The SIRT1/PGC-1αaxis,which was downregulated in the model group,was upregulated by EA intervention.The endogenous antioxidant system related to the SIRT1/PGC-1αaxis,previously inhibited in diabetic rats,was reactivated.A similar trend was observed in inflammatory markers.When SIRT1 was inhibited in diabetic rats,these beneficial effects were abolished.CONCLUSION EA can alleviate the symptoms of T2DNP in experimental rats,and its effects may be related to the mitochondrial biogenesis and endogenous antioxidant system mediated by the SIRT1/PGC-1αaxis.
关 键 词:ELECTROACUPUNCTURE Type 2 diabetic peripheral neuropathy Silent matching type information regulation 2 homolog-1/peroxisome proliferator-activated receptor-gamma coactivator-1αaxis Mitochondria biogenesis Oxidative stress
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...