Journal of diabetes research · 2026
Electroacupuncture Attenuates Peripheral Neuropathy Development in Hyperglycemic Rats and Is Associated With NLRP3 Inflammasome Modulation.
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Zhu Ziyue, Zou Qinglan, Su Chengguo, You Xi, Zeng Weijian, Li Nanxi, Thitinun Bumrungtham, Li Ying, Yao Junpeng, Zhang Wei
Аннотация
BACKGROUND: This study employed a high-energy diet and streptozotocin (STZ) injection to establish a rat model of diabetic peripheral neuropathy (DPN), focusing on inflammatory responses. The aim was to investigate the mechanism by which electroacupuncture (EA) improves the neuroinflammatory microenvironment in diabetic rats and attenuates DPN development.
METHOD: Twenty-four male SD rats were randomly assigned using a random number table into control, model, and EA groups, with eight rats in each group. A DPN model was established using a high-energy diet combined with STZ injection. The EA group received intervention immediately after successful diabetic modeling, whereas intervention ceased once DPN modeling was established in the model group. During the intervention period, random blood glucose levels and paw withdrawal latency (PWL) were recorded weekly for rats in each group. After intervention, the neurophysiological status of rats was assessed. The ultrastructure of Schwann cells in the sciatic nerve was observed using transmission electron microscopy. Western Blot and RT-PCR were employed to detect the protein levels and mRNA expression of ASC, caspase-1, NLRP3, and P62. ELISA was implemented to measure IL-18 and IL-1β levels.
RESULTS: Compared with the control, model rats exhibited significantly elevated random blood glucose and PWL levels (p < 0.0001, p < 0.0001), markedly reduced motor nerve conduction velocity (MNCV) (p < 0.0001), and pronounced damage to Schwann cell structure. ASC, caspase-1, NLRP3, and P62 levels were markedly elevated (p < 0.01, p < 0.0001, p < 0.0001, p < 0.001; p < 0.001, p < 0.01, p < 0.05, p < 0.001), whereas IL-18 and IL-1β levels were notably elevated (p < 0.0001, p < 0.0001). Compared with the model group, rats in the EA group displayed no marked difference in random blood glucose (p > 0.05), but reduced PWL (p < 0.0001), increased MNCV (p < 0.0001), and milder structural damage to Schwann cells. ASC, caspase-1, NLRP3, and P62 levels were considerably reduced (p < 0.01, p < 0.0001, p < 0.001, p < 0.001; p < 0.05, p < 0.05, p < 0.05, p < 0.05), whereas IL-18 and IL-1β levels were notably diminished (p < 0.001, p < 0.0001).
CONCLUSION: EA may protect peripheral nerve tissue morphology and function by suppressing NLRP3 inflammasomes, thereby alleviating inflammatory responses and potentially attenuating the onset and progression of DPN. This process may be associated with autophagy; but further mechanistic studies are needed to establish causality.
METHOD: Twenty-four male SD rats were randomly assigned using a random number table into control, model, and EA groups, with eight rats in each group. A DPN model was established using a high-energy diet combined with STZ injection. The EA group received intervention immediately after successful diabetic modeling, whereas intervention ceased once DPN modeling was established in the model group. During the intervention period, random blood glucose levels and paw withdrawal latency (PWL) were recorded weekly for rats in each group. After intervention, the neurophysiological status of rats was assessed. The ultrastructure of Schwann cells in the sciatic nerve was observed using transmission electron microscopy. Western Blot and RT-PCR were employed to detect the protein levels and mRNA expression of ASC, caspase-1, NLRP3, and P62. ELISA was implemented to measure IL-18 and IL-1β levels.
RESULTS: Compared with the control, model rats exhibited significantly elevated random blood glucose and PWL levels (p < 0.0001, p < 0.0001), markedly reduced motor nerve conduction velocity (MNCV) (p < 0.0001), and pronounced damage to Schwann cell structure. ASC, caspase-1, NLRP3, and P62 levels were markedly elevated (p < 0.01, p < 0.0001, p < 0.0001, p < 0.001; p < 0.001, p < 0.01, p < 0.05, p < 0.001), whereas IL-18 and IL-1β levels were notably elevated (p < 0.0001, p < 0.0001). Compared with the model group, rats in the EA group displayed no marked difference in random blood glucose (p > 0.05), but reduced PWL (p < 0.0001), increased MNCV (p < 0.0001), and milder structural damage to Schwann cells. ASC, caspase-1, NLRP3, and P62 levels were considerably reduced (p < 0.01, p < 0.0001, p < 0.001, p < 0.001; p < 0.05, p < 0.05, p < 0.05, p < 0.05), whereas IL-18 and IL-1β levels were notably diminished (p < 0.001, p < 0.0001).
CONCLUSION: EA may protect peripheral nerve tissue morphology and function by suppressing NLRP3 inflammasomes, thereby alleviating inflammatory responses and potentially attenuating the onset and progression of DPN. This process may be associated with autophagy; but further mechanistic studies are needed to establish causality.