scholarly journals Atorvastatin suppresses NLRP3 inflammasome activation in intracerebral hemorrhage via TLR4- and MyD88-dependent pathways

Aging ◽  
2022 ◽  
Author(s):  
Duo Chen ◽  
Lu Sui ◽  
Cao Chen ◽  
Sanchuan Liu ◽  
Xianfeng Sun ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

Cordycepin confers neuroprotection in mice models of intracerebral hemorrhage via suppressing NLRP3 inflammasome activation

2017 ◽  
Vol 32 (4) ◽  
pp. 1133-1145 ◽  
Author(s):  
Yijun Cheng ◽  
Yongxu Wei ◽  
Wenlei Yang ◽  
Yaying Song ◽  
Hanbing Shang ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage

2017 ◽  
Vol 93 ◽  
pp. 308-315 ◽  
Author(s):  
Raorao Yuan ◽  
Hengyi Fan ◽  
Shiqi Cheng ◽  
WeiWei Gao ◽  
Xin Xu ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals iTRAQ-Based Quantitative Proteomics Indicated Nrf2/OPTN-Mediated Mitophagy Inhibits NLRP3 Inflammasome Activation after Intracerebral Hemorrhage

2021 ◽  
Vol 2021 ◽  
pp. 1-26
Author(s):  
Yijun Cheng ◽  
Mingjian Liu ◽  
Hao Tang ◽  
Bin Chen ◽  
Guoyuan Yang ◽  
...  
Keyword(s):  
Survival Rate ◽  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Nlrp3 Inflammasome ◽  
Neuronal Death ◽  
Inflammasome Activation ◽  
Secondary Brain Injury ◽  
Clear Understanding ◽  
Hematoma Volume ◽  
Nlrp3 Inflammasome Activation

Intracerebral hemorrhage- (ICH-) induced secondary brain injury (SBI) is a very complex pathophysiological process. However, the molecular mechanisms and drug targets of SBI are highly intricate and still elusive, yet a clear understanding is crucial for the treatment of SBI. In the current study, we aimed to confirm that nuclear factor-E2-related factor 2 (Nrf2)/Optineurin- (OPTN-) mediated mitophagy alleviated SBI by inhibiting nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3) inflammasome activation based on the isobaric tag for relative and absolute quantization (iTRAQ) quantification proteomics. Human ICH brain specimens were collected for iTRAQ-based proteomics analysis. Male Nrf2 wild-type (WT) and knockout (KO) mice were employed to establish ICH murine models. The survival rate, hematoma volume, neurofunctional outcomes, blood-brain barrier (BBB) permeability, brain edema, spatial neuronal death, NLRP3 inflammasome, inflammatory response, mitochondrial function, and mitophagy level were evaluated after ICH. The iTRAQ quantification analysis showed that the differentially expressed proteins (DEPs), Nrf2 and NLRP3, were closely associated with the initiation and development of SBI after ICH. The Nrf2 KO mice had a significantly lower survival rate, bigger hematoma volume, worse neurological deficits, and increased BBB disruption, brain edema, and neuronal death when compared with the Nrf2 WT mice after ICH. Furthermore, Nrf2 KO enhanced NLRP3 inflammasome activation and neuroinflammation as evidenced by the NF-κB activation and various proinflammatory cytokine releases following ICH. Moreover, Nrf2 could interact with and modulate the mitophagy receptor OPTN, further mediating mitophagy to remove dysfunctional mitochondria after ICH. Furthermore, OPTN small interfering RNA (siRNA) increased the NLRP3 inflammasome activation by downregulating mitophagy level and enhancing mitochondrial damage in the Nrf2 WT mice after ICH. Together, our data indicated that Nrf2/OPTN inhibited NLRP3 inflammasome activation, possibly via modulating mitophagy, therefore alleviating SBI after ICH.

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