Dataset Information

Transcriptomics and experiments verified that astaxanthin reduces the apoptosis of nerve cells in ischemic stroke by inhibiting the toll-like receptor signaling pathway

ABSTRACT: Background and Objective. Inflammation is an important pathological process in ischemic stroke (IS). Astaxanthin (ATX) is a natural product with neuroprotection effects. However, the mechanism of ATX on anti-inflammatory after IS is not clear. The aim of this study was to investigate the mechanism of ATX on anti-inflammatory after IS. Methods. Male Sprague-Dawley rats were used to establish a model of middle cerebral artery occlusion (MCAO) on one side, and were pre-treated with gavage of ATX for 7 days. One day after MCAO, the brain tissues were collected. Transcriptomic sequencing, flow cytometry, brain water content, western blot, HE staining and ELISA were analyzed to evaluated the brain damage. Results. ATX treatment has improved the neurological deficits, reduced brain edema, and apoptosis. Also, ATX has reduced inflammation and apoptosis related proteins such as TLR4, MyD88, NFκB, IL1β, IL6, Cyt C and Caspsae3. Conclusions. ATX can improve nerve damage after IS, and these protective effects were realized by anti-inflammatory and anti-apoptosis. This protective mechanism involves the TLR4/MyD88/NF-κB signaling pathway

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE324069 | GEO | 2026/03/10

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Toll-like receptors (TLRs) are important mediators of chronic inflammation in numerous autoimmune diseases, although the role of these receptors in primary Sjögren’s syndrome (pSS) remains incompletely understood. Previous studies in our laboratory established Myd88 as a crucial mediator of disease, although the upstream signaling events that culminate in Myd88 activation have yet to be identified. To objective of this study was to identify specific Myd88-dependent TLR-related pathways that are dysregulated both locally and systemically in a mouse model of pSS (NOD.B10Sn-H2b/J (NOD.B10)). We performed RNA-sequencing on spleens derived from NOD.B10 mice. We then harvested salivary tissue and spleens from Myd88-sufficient and deficient C57BL/10 (BL/10) and NOD.B10 mice and performed flow cytometry to determine expression of Myd88-dependent TLRs. We then cultured splenocytes with TLR2 and TLR4 agonists and measured IL-6 secretion by ELISA. Next, we evaluated spontaneous and TLR4-mediated inflammatory cytokine secretion in NOD.B10 salivary tissue. Finally, we assessed spontaneous Myd88-dependent cytokine secretion by NOD.B10 salivary cells. We identified dysregulation of numerous TLR-related networks in pSS splenocytes, particularly those employed by TLR2 and TLR4. We found upregulation of TLRs in both the splenic and salivary tissue from pSS mice. In NOD.B10 splenic tissue, B cell TLR1, TLR2, and TLR6 expression was reduced to levels of BL/10 controls in the absence of Myd88. Splenocytes from NOD.B10 mice were hyper-responsive to TLR2 ligation and the endogenous molecule decorin modulated inflammation via TLR4. Finally, we found spontaneous secretion of numerous inflammatory cytokines and this was enhanced following TLR4 ligation in female NOD.B10 salivary tissue as compared to males. Moreover, we found that spontaneous production of salivary IL-6, MCP-1 and TNFa requires Myd88 in pSS salivary tissue. Thus, our data demonstrate that Myd88-dependent TLR pathways contribute to the inflammatory landscape in pSS, and inhibition of such will likely have therapeutic utility.

Dataset Information

Transcriptomics and experiments verified that astaxanthin reduces the apoptosis of nerve cells in ischemic stroke by inhibiting the toll-like receptor signaling pathway

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets