Adiponectin reduces brain injury after intracerebral hemorrhage by reducing NLRP3 inflammasome expression

Wang, Shaohua; Yao, Qiuhui; Wan, Yu; Wang, Jieqiong; Huang, Conggai; Li, Dan; Yang, Bo

doi:10.1080/00207454.2019.1679810

Cited by 28 publications

(16 citation statements)

References 28 publications

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“…It has confirmed adiponectin has beneficial effects by increasing insulin sensitivity, keeping blood glucose concentration and lipid distribution, and reducing atherosclerosis and inflammation [ 24 ]. According to the recent study, adiponectin reduces brain injury after intracerebral hemorrhage by reducing NLRP3 inflammasome expression [ 25 ]. Evidence showed that adiponectin promoted neural survival following ICH injury in the diabetic setting [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Activation of AdipoR1 with rCTRP9 Preserves BBB Integrity through the APPL1/AMPK/Nrf2 Signaling Pathway in ICH Mice

Zhao

Kong²,

Gong

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. The disruption of the blood brain barrier (BBB) is the key factor leading to neurological impairment after intracerebral hemorrhage (ICH) injury. Adiponectin receptor 1 (AdipoR1) has an important effect contributing to the integrity of BBB. As a homologue of adiponectin, recombinant C1q/TNF-related protein 9 (rCTRP9) has neuroprotective effect in cerebrovascular diseases. The aim of this study was to investigate the protective effect of AdipoR1 activation with rCTRP9 on BBB integrity after ICH injury and the potential mechanisms. Methods. 177 male mice were subjected in this study. ICH was induced by injecting collagenase into the right basal ganglia. rCTRP9 was treated intranasally at 1 hour after ICH. Selective siRNA was administered prior to ICH. Western blot, immunofluorescence staining, neurobehavioral tests, and BBB permeability were evaluated. Results. ICH increased the expression of endogenous AdipoR1 and CTRP9. Administration of rCTRP9 ameliorated neurological deficits and reduced the BBB permeability at 24 hours in ICH mice. Furthermore, rCTRP9 promoted the expression of AdipoR1, APPL1, p-AMPK, Nrf2, and tight junctional proteins. The intervention of specific siRNA of AdipoR1, APPL1, and p-AMPK reversed the protective effects of rCTRP9. Conclusions. Activation of AdipoR1 with rCTRP9 improved neurological functions and preserved BBB integrity through the APPL1/AMPK/Nrf2 signaling pathway in ICH mice. Therefore, CTRP9 could serve as a promising therapeutic method to alleviate BBB injury following ICH in patients.

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Section: Discussionmentioning

confidence: 99%

Activation of AdipoR1 with rCTRP9 Preserves BBB Integrity through the APPL1/AMPK/Nrf2 Signaling Pathway in ICH Mice

Zhao

Kong²,

Gong

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Cleaved caspase-1, which could be activated by NLRP3 inflammasome, a large intracellular multiprotein complex containing caspase-1, ASC and NLRP3, is crucial for the transformation of IL-1β and IL-18 from precursor form to mature form, which could further trigger the downstream signaling pathways [ 38 , 39 ]. It has been reported that MCC950, a kind of the NLRP3 inflammasome inhibitor, could against neuroinflammation and had a neuroprotective effect which might be associated with reduced activation of microglial, recruitment of leukocyte, and production of pro-inflammatory cytokines [ 40 , 41 ]. Besides, researchers found that blocking NLRP3 function in vivo significantly delayed neuronal degeneration and ataxia onset in severe neurodegenerative diseases, such as cerebellar ataxias [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

RKC-B1 Blocks Activation of NF-κB and NLRP3 Signaling Pathways to Suppress Neuroinflammation in LPS-Stimulated Mice

et al. 2021

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RKC-B1 is a novel fermentation product obtained from the marine micromonospora FIM02-523A. Thus far, there have been few reports about the pharmacological activity of RKC-B1. In our present study, we investigated the anti-neuroinflammatory effects and the possible mechanism of RKC-B1 in LPS-stimulated mice. After treatment with RKC-B1, RNA-seq transcriptome of the cerebral cortex tissue was conducted to find the differentially expressed genes (DEGs). Inflammatory cytokines and proteins were evaluated by ELISA and WB. In RNA-seq analysis, there were 193 genes screened as core genes of RKC-B1 for treatment with neuroinflammation. The significant KEGG enrichment signaling pathways of these core genes were mainly included TNF signaling pathway, IL-17 signaling pathway, NOD-like receptor signaling pathway, NF-κB signaling pathway and others. The corresponding top five KEGG enrichment pathways of three main clusters in PPI network of core genes were closely related to human immune system and immune disease. The results showed that RKC-B1 reduced the levels of pro-inflammatory factors (IL-6, IL-1β, MCP-1, and ICAM-1) and the expression of COX2 in cerebral cortex tissue. Additionally, we found that the anti-neuroinflammation activity of RKC-B1 might be related to suppress activating of NF-κB and NLRP3/cleaved caspase-1 signaling pathways. The current findings suggested that RKC-B1 might be a promising anti-neuroinflammatory agent.

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“…Each rat's performance was calculated as the mean score of three trials. In the wire hanging test ( 24 ), the rats were placed in the center of a 600 x 2 mm wire 50 cm from the ground with a sponge pad underneath. Each rat was observed four times for 30 sec each.…”

Section: Methodsmentioning

confidence: 99%

Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats

et al. 2021

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Adiponectin reduces brain injury after intracerebral hemorrhage by reducing NLRP3 inflammasome expression

Cited by 28 publications

References 28 publications

Activation of AdipoR1 with rCTRP9 Preserves BBB Integrity through the APPL1/AMPK/Nrf2 Signaling Pathway in ICH Mice

Activation of AdipoR1 with rCTRP9 Preserves BBB Integrity through the APPL1/AMPK/Nrf2 Signaling Pathway in ICH Mice

RKC-B1 Blocks Activation of NF-κB and NLRP3 Signaling Pathways to Suppress Neuroinflammation in LPS-Stimulated Mice

Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats

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