Electroacupuncture Ameliorates Neuronal Injury by NLRP3/ASC/Caspase-1 Mediated Pyroptosis in Cerebral Ischemia-Reperfusion

Tang, Bin; Li, Yan; Xu, Xifa; Du, Guangzhong; Wang, Huanyuan

doi:10.1007/s12035-023-03712-1

Cited by 9 publications

(2 citation statements)

References 32 publications

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“…Hence, our investigation examined if TEAS exhibited defensive properties and further explored the associated mechanisms during the initial stage of ischemic stroke. In previous studies, EA played a protective role in ischemic stroke by regulating apoptosis, inflammation, pyroptosis and other pathological processes (Xing et al, 2018b;Tang et al, 2023). EA treatment at Baihui and Hegu acupoints has been shown to mitigate cerebral ischemic injury (Jiang et al, 2017).…”

Section: Discussionmentioning

confidence: 96%

Transcutaneous electrical acupoint stimulation alleviates cerebral ischemic injury through the TLR4/MyD88/NF-κ B pathway

Wu,

Tan,

et al. 2024

Front. Cell. Neurosci.

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This study was to explore whether transcutaneous electrical acupoint stimulation (TEAS) treatment could mediate inflammation, apoptosis, and pyroptosis of neuronal cells and microglia activation through the TLR4/MyD88/NF-κB pathway in the early stage of ischemic stroke. TEAS treatment at Baihui (GV20) and Hegu (LI4) acupoints of the affected limb was administered at 24, 48, and 72 h following middle cerebral artery occlusion/reperfusion (MCAO/R), with lasting for 30 min each time. Neurological impairment scores were assessed 2 h and 72 h after ischemia/reperfusion (I/R). TTC staining was used to evaluate the volume of brain infarction. The histopathologic changes of hippocampus were detected by H&E staining. WB analysis was performed to assess the levels of TLR4, MyD88, p-NF-κB p65/NF-κB p65, and inflammation, apoptosis, pyroptosis-related proteins. TLR4 expression was measured using immunohistochemistry. The expression of inflammation-related proteins was also measured using ELISA. Immunofluorescence was used to detect the expression level of Iba1. Our findings demonstrated that TEAS intervention after I/R improved neurological function, reduced the volume of brain infarction, and mitigated pathological damage. Moreover, TEAS reduced the levels of TLR4, MyD88, p-NF-κB p65/NF-κB p65, TNF-α, IL-6, Bax, NLRP3, cleaved caspase-1/pro caspase-1, IL-1β, IL-18, GSDMD, and Iba1 while enhancing Bcl-2 expression. Moreover, the protective effects of TEAS could be counteracted by lipopolysaccharide (LPS, a TLR4 agonist). In conclusion, TEAS can reduce cerebral damage and suppress inflammation, cell death, and microglia activation after ischemic stroke via inhibiting the TLR4/MyD88/NF-κB pathway.

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Section: Discussionmentioning

confidence: 96%

Transcutaneous electrical acupoint stimulation alleviates cerebral ischemic injury through the TLR4/MyD88/NF-κ B pathway

Wu,

Tan,

et al. 2024

Front. Cell. Neurosci.

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“…These slices were then placed in a 2% TTC solution prepared with TTC powder at 37 °C for 30 min. Normal brain tissue appeared red, while ischemic brain tissue appeared white ( Tang et al, 2024 ). The total area of the infarct in each section was calculated and presented as a percentage of the volume of the unaffected area: infarct volume (%) = [(volume of the healthy side hemisphere - volume of the uninjured area on the affected side)/volume of the healthy side hemisphere] × 100%.…”

Section: Methodsmentioning

confidence: 99%

Exosomes derived from HUVECs alleviate ischemia-reperfusion induced inflammation in neural cells by upregulating KLF14 expression

Qin,

Zhou,

et al. 2024

Front. Pharmacol.

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Neuroinflammation plays a key role in the progression of secondary brain injury after ischemic stroke, and exosomes have been increasingly recognized to eliminate inflammatory responses through various mechanisms. This study aimed to explore the effect and possible mechanism of human umbilical vein endothelial cells derived exosomes (H-EXOs) on neuroinflammation. We established a transient middle cerebral artery occlusion/reperfusion (tMCAO/R) in male rats and oxygen-glucose-deprivation/reoxygenation (OGD/R) model in cultured neurons to mimic secondary brain injury after ischemic stroke in vivo. H-EXOs were administered at the same time of reperfusion. Results showed that the production of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, and the transcription factor Krüppel-like factor 14 (KLF14) were significantly increased both in rat brain tissue and cultured neural cells after ischemic-reperfusion (I/R) injury. H-EXOs treatment significantly improved the cultured cell viability, reduced infarct sizes, mitigated neurobehavioral defects, and alleviated the expression of pro-inflammatory cytokines compared with the control group, indicating that H-EXOs exerted anti-inflammatory effect against I/R injury. Further studies revealed that the anti-inflammatory effect of H-EXOs could be weakened by small-interfering RNA (siKLF4) transfection. KLF14 was a protective factor produced during cerebral ischemia-reperfusion injury. In conclusion, H-EXOs protect neurons from inflammation after I/R injury by enhancing KLF14 expression.

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BAK ameliorated cerebral infarction/ischemia–reperfusion injury by activating AMPK/Nrf2 to inhibit TXNIP/NLRP3/caspase-1 axis

Xu,

Yao,

Gao

et al. 2025

Neuroscience Letters

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Electroacupuncture Ameliorates Neuronal Injury by NLRP3/ASC/Caspase-1 Mediated Pyroptosis in Cerebral Ischemia-Reperfusion

Cited by 9 publications

References 32 publications

Transcutaneous electrical acupoint stimulation alleviates cerebral ischemic injury through the TLR4/MyD88/NF-κ B pathway

Transcutaneous electrical acupoint stimulation alleviates cerebral ischemic injury through the TLR4/MyD88/NF-κ B pathway

Exosomes derived from HUVECs alleviate ischemia-reperfusion induced inflammation in neural cells by upregulating KLF14 expression

BAK ameliorated cerebral infarction/ischemia–reperfusion injury by activating AMPK/Nrf2 to inhibit TXNIP/NLRP3/caspase-1 axis

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