Published online Feb 15, 2025. doi: 10.4239/wjd.v16.i2.93130
Revised: September 15, 2024
Accepted: October 31, 2024
Published online: February 15, 2025
Processing time: 313 Days and 23.1 Hours
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 coac
To validate the effectiveness of electroacupuncture (EA) in the treatment of T2DPN and investigate its potential mechanism based on the SIRT1/PGC-1α axis.
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-1α axis, 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.
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-1α axis, which was downregulated in the model group, was upregulated by EA intervention. The endogenous antioxidant system related to the SIRT1/PGC-1α axis, 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.
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-1α axis.
Core Tip: Diabetic peripheral neuropathy (DPN) is thought to be linked to the vicious cycle of oxidative stress and mitochondrial dysfunction triggered by metabolic abnormalities. Electroacupuncture is commonly used as an adjuvant therapy for DPN in clinical practice, though its precise mechanism remains unclear. A rat model of DPN was established by combining a high-fat diet with streptozotocin injection. The final results suggest that the beneficial effects of electroacupuncture on DPN rats may be related to the regulation of the silent information regulator type 2 homolog-1/peroxisome proliferator-activated receptor-gamma coactivator-1α axis, which activates mitochondrial biogenesis and reduces oxidative stress and protects intact mitochondria.