Pien-Tze-Huang, a Chinese patent formula, attenuates NLRP3 inflammasome-related neuroinflammation by enhancing autophagy via the AMPK/mTOR/ULK1 signaling pathway

Huang, Zhenwei; Zhou, Xian; Zhang, Xiaoqin; Huang, Lili; Sun, Yibin; Cheng, Zaixing; Xu, Wen; Li, Chun Guang; Zheng, Yanfang; Huang, Mingqing

doi:10.1016/j.biopha.2021.111814

Cited by 42 publications

(19 citation statements)

References 39 publications

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“…Autophagy is regulated primarily by mTOR and AMPK, and a key regulator of autophagosome formation is ULK1. AMPK promotes autophagy by phosphorylating ULK1, whereas mTOR inhibits autophagy by inhibiting ULK1 phosphorylation [ 37 , 38 ]. AMPK-mediated inhibition of ULK1 involves two mechanisms: direct inhibition of phosphorylated ULK1 by AMPK and indirect inhibition of ULK1 phosphorylation by activating mTOR phosphorylation [ 39 , 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

Around-the-Clock Noise Induces AD-like Neuropathology by Disrupting Autophagy Flux Homeostasis

Zheng

She²,

Wang

et al. 2022

Cells

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Environmental noise is a common hazard in military operations. Military service members during long operations are often exposed to around-the-clock noise and suffer massive emotional and cognitive dysfunction related to an Alzheimer’s disease (AD)-like neuropathology. It is essential to clarify the mechanisms underlying the effects of around-the-clock noise exposure on the central nervous system. Here, Wistar rats were continuously exposed to white noise (95 dB during the on-duty phase [8:00–16:00] and 75 dB during the off-duty phase (16:00–8:00 the next day)) for 40 days. The levels of phosphorylated tau, amyloid-β (Aβ), and neuroinflammation in the cortex and hippocampus were assessed and autophagosome (AP) aggregation was observed by transmission electron microscopy. Dyshomeostasis of autophagic flux resulting from around-the-clock noise exposure was assessed at different stages to investigate the potential pathological mechanisms. Around-the-clock noise significantly increased Aβ peptide, tau phosphorylation at Ser396 and Ser404, and neuroinflammation. Moreover, the AMPK-mTOR signaling pathway was depressed in the cortex and the hippocampus of rats exposed to around-the-clock noise. Consequently, autophagosome–lysosome fusion was deterred and resulted in AP accumulation. Our results indicate that around-the-clock noise exposure has detrimental influences on autophagic flux homeostasis and may be associated with AD-like neuropathology in the cortex and the hippocampus.

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Section: Discussionmentioning

confidence: 99%

Around-the-Clock Noise Induces AD-like Neuropathology by Disrupting Autophagy Flux Homeostasis

Zheng

She²,

Wang

et al. 2022

Cells

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“…Besides, enhanced microglial autophagy has been demonstrated to suppress the activation of NLRP3 inflammasome in LPS-treated BV2 microglia ( Espinosa-Garcia et al, 2020 ). Huang et al also verified that enhanced autophagy via AMPK/mTOR/ULK1 pathway could suppress NLRP3 inflammasome-mediated neuroinflammation in LPS-treated BV2 microglia ( Huang Z. et al, 2021 ). The therapeutic promise of inhibiting NLRP3 inflammasome activation by regulating microglial autophagy in cerebrovascular diseases has attracted increasing attention.…”

Section: Interaction Between Microglial Autophagy and Other Biologica...mentioning

confidence: 94%

“…Several intracellular molecules such as PARP14 (a member in the Poly (ADP-ribose) polymerase superfamily) and PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1α) have been demonstrated to limit microglial activation and promote neurological recovery after stroke by inducing microglial autophagy ( Han et al, 2021 ; Tang et al, 2021 ). Some drugs such as SB216763 (the serine/threonine kinase GSK-3β inhibitor) and Pien-Tze-Huang (a patent formula in the Chinese Pharmacopoeia for the treatment of inflammatory diseases) have also been found to suppress microglial over-activation and inflammatory response by inducing microglial autophagy in ischemic stroke ( Zhou et al, 2011 ; Huang Z. et al, 2021 ; Tang et al, 2021 ). Xia et al found that following OGD/R injury, blocking autophagic flux induced the transition of BV2 microglia toward a pro-inflammatory phenotype, which increases the release of proinflammatory cytokines and contributes to neuroinflammation ( Xia et al, 2016 ).…”

Section: Interaction Between Microglial Autophagy and Other Biologica...mentioning

confidence: 99%

Microglial autophagy in cerebrovascular diseases

Chen

Zhang

Chu

et al. 2022

Front. Aging Neurosci.

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Microglia are considered core regulators for monitoring homeostasis in the brain and primary responders to central nervous system (CNS) injuries. Autophagy affects the innate immune functions of microglia. Recently some evidence suggests that microglial autophagy is closely associated with brain function in both ischemic stroke and hemorrhagic stroke. Herein, we will discuss the interaction between autophagy and other biological processes in microglia under physiological and pathological conditions and highlight the interaction between microglial metabolism and autophagy. In the end, we focus on the effect of microglial autophagy in cerebrovascular diseases.

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“…DJ-1 interference combined with a Sirt1 inhibitor increased the effect of DJ-1 interference on microglial polarization from anti-inflammatory to pro-inflammatory states, decreased the level of the Atg5-Atg12-Atg16L1 complex, and inhibited autophagy during cerebral I/R injury (170). Activation of autophagy via the AMPK pathway could facilitate microglial anti-inflammatory activation and exert neuroprotective effects during an inflammatory process (171)(172)(173)(174)(175). P2X7 receptor can activate AMPK pathways in the regulation of mitochondrial and lysosomal functions in microglia (176,177).…”

Section: Microglia Autophagy Regulates Inflammatory Responses In Isch...mentioning

confidence: 99%

Microglia autophagy in ischemic stroke: A double-edged sword

Peng

Yao

et al. 2022

Front. Immunol.

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Ischemic stroke (IS) is one of the major types of cerebrovascular diseases causing neurological morbidity and mortality worldwide. In the pathophysiological process of IS, microglia play a beneficial role in tissue repair. However, it could also cause cellular damage, consequently leading to cell death. Inflammation is characterized by the activation of microglia, and increasing evidence showed that autophagy interacts with inflammation through regulating correlative mediators and signaling pathways. In this paper, we summarized the beneficial and harmful effects of microglia in IS. In addition, we discussed the interplay between microglia autophagy and ischemic inflammation, as along with its application in the treatment of IS. We believe this could help to provide the theoretical references for further study into IS and treatments in the future.

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Pien-Tze-Huang, a Chinese patent formula, attenuates NLRP3 inflammasome-related neuroinflammation by enhancing autophagy via the AMPK/mTOR/ULK1 signaling pathway

Cited by 42 publications

References 39 publications

Around-the-Clock Noise Induces AD-like Neuropathology by Disrupting Autophagy Flux Homeostasis

Around-the-Clock Noise Induces AD-like Neuropathology by Disrupting Autophagy Flux Homeostasis

Microglial autophagy in cerebrovascular diseases

Microglia autophagy in ischemic stroke: A double-edged sword

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