Neurological research · 2025
SIRT1 activates autophagy through Smad3 deacetylation and inhibits microglia activation to relieve SCI.
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Chen Hongbo, Li Rongmei, Li Ya, Hong Baocai, Fu Xiongli, Tu Pinwen, Yang Chaochao, Deng Yongqian, Zhang Yang, Lv Shaokun
Аннотация
BACKGROUND: In the state of spinal cord injury (SCI), microglia over-activate and release inflammatory factors, which aggravate SCI. The neuroprotective factor known as sirtuin 1 (SIRT1) is intricately linked to the activation of BV2. This research examined the influence of SIRT1-regulated activation of BV2 on SCI.
METHODS: Activation of BV2 cells was triggered by lipopolysaccharide (LPS), and a SCI rat model was created using laminectomy. The condition of SCI in the rats was assessed through HE and Nissl staining. The levels of related genes and proteins were detected by RT-qPCR, ELISA, western blotting, and immunofluorescence.
RESULTS: Our findings demonstrated that following SCI, there was an increase in microglial activation alongside a notable decrease in SIRT1 expression. The overexpression of SIRT1 effectively reduced microglial activation. Investigations into the molecular mechanisms indicated that SIRT1 exerts its effects by inhibiting Smad3 via deacetylation, and promotes autophagy, which in turn helps to reduce microglial activation and mitigate the progression of SCI. Moreover, impairing autophagy was observed to enhance microglial activation. Additionally, in vivo studies illustrated that the activation of SIRT1 can improve the underlying pathophysiology of SCI.
CONCLUSION: SIRT1 activates autophagy through Smad3 deacetylation and inhibits microglia activation to relieve SCI.
METHODS: Activation of BV2 cells was triggered by lipopolysaccharide (LPS), and a SCI rat model was created using laminectomy. The condition of SCI in the rats was assessed through HE and Nissl staining. The levels of related genes and proteins were detected by RT-qPCR, ELISA, western blotting, and immunofluorescence.
RESULTS: Our findings demonstrated that following SCI, there was an increase in microglial activation alongside a notable decrease in SIRT1 expression. The overexpression of SIRT1 effectively reduced microglial activation. Investigations into the molecular mechanisms indicated that SIRT1 exerts its effects by inhibiting Smad3 via deacetylation, and promotes autophagy, which in turn helps to reduce microglial activation and mitigate the progression of SCI. Moreover, impairing autophagy was observed to enhance microglial activation. Additionally, in vivo studies illustrated that the activation of SIRT1 can improve the underlying pathophysiology of SCI.
CONCLUSION: SIRT1 activates autophagy through Smad3 deacetylation and inhibits microglia activation to relieve SCI.