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Protection of TLR5 agonist, CBLB502, against cisplatin treated mouse liver and kidney

ABSTRACT: Protection of TLR5 agonist, CBLB502, against cisplatin treated mouse liver and kidney

PROVIDER: PRJNA866554 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20871805_1.fastq.gz	Fastqsanger.gz
	SRR20871805_2.fastq.gz	Fastqsanger.gz
	SRR20871806_1.fastq.gz	Fastqsanger.gz
	SRR20871806_2.fastq.gz	Fastqsanger.gz
	SRR20871807_1.fastq.gz	Fastqsanger.gz

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Protection of TLR5 agonist, CBLB502, against cisplatin treated mouse liver and kidney

Project description:TLR5 agonist CBLB502 has been reported playing protective effects again IR, Here we find CBLB502 might protect cis-platin induced liver and kidney damages.

2023-08-01 | GSE210655 | GEO

Pregnane X Receptor (PXR) protects against cisplatin-induced acute kidney injury

Project description:Background: Cisplatin-induced acute kidney injury (CAKI) has been recognized as one of the most serious side effects of cisplatin. Pregnane X receptor (PXR) is a ligand-dependent nuclear receptor and serves as a master regulator of xenobiotic detoxification. Increasing evidence also suggests PXR has many nonxenobiotic functions including the regulation of cell proliferation, inflammatory response and glucose and lipid metabolism. Methods: In this study, we aimed to investigate the role of PXR in cisplatin-induced nephrotoxicity. CAKI model was performed in wild-type or PXR knockout mice. Pregnenolone 16α-carbonitrile (PCN), a mouse PXR specific agonist, was used for PXR activation. The renal function, biochemical, histopathological and molecular alterations were examined in mouse blood, urine or renal tissues. Whole transcriptome analysis was performed by RNA sequencing. Dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays were applied to determine the regulation of PXR on its target genes. Results: We found that PXR activation significantly attenuated CAKI as reflected by improved renal function, reduced renal tubular apoptosis, ameliorated oxidative and endoplasmic reticulum stress, and suppressed inflammatory factor expression. RNA sequencing analysis revealed that the renoprotective effect of PXR was associated with multiple crucial signaling pathways. In particular, PXR protected against cisplatin-induced AKI by the activation of PI3K/AKT pathway and the induction of multidrug and toxin extrusion 1 (MATE1), an important transporter mediating cellular excretion of cisplatin, in the kidney. Conclusions: Our results demonstrate that PXR activation can preserve renal function in cisplatin-induced AKI and suggest a possibility of PXR as a novel therapeutic target for cisplatin-induced nephrotoxicity.

2023-03-20 | GSE147256 | GEO

Project description:Protection of TLR5 agonist, CBLB502, against cisplatin treated mouse liver and kidney

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Project description:HEK293 cells overexpressing TLR5 (TLR5+) and parent cell lines were infected with H. pylori to differentiate the gene expression through increased TLR5 signalling.

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Synergistic hepatoprotective effect of the TLR5 agonist CBLB502 and its downstream effector IL-22

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Kidney-targeted renalase agonist prevents cisplatin-induced chronic kidney disease by inhibiting regulated necrosis and inflammation

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Project description:Profiling of proteolytic events mouse kidneys during cisplatin-induced kidney damage. Kidneys from vehicle-treated mice are compared to cisplatin-treated mice and cisplatin treatment in animals preconditioned by hypoxia or calory restriction regimes.

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Prevention and cure of rotavirus infection via TLR5/NLRC4-mediated production of IL-22 and IL-18

Project description:Activators of innate immunity may have potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin (IL)-22, which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection, and thus holds promise as a broad-spectrum antiviral agent.

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Toll-like receptor agonist CBLB502 protects against radiation-induced intestine injury in mice

Project description:Radiation-induced intestinal injury is one of the most common complications of abdominal and pelvic radiotherapy. Severe intestinal injury caused by ionizing radiation (IR) has a high mortality rate, which is a worldwide problem requiring urgent attention. IR can cause intestinal tissue damage, inflammatory cell infiltration and pro-inflammatory cytokine release. However, methods to protect against radiation-induced intestinal injury are limited. CBLB502, a Toll-like receptor 5 (TLR5) agonist from Salmonella flagellin, has radioprotective effects on various tissues and organs. In order to further explore the molecular mechanism of IR-induced intestinal injury and the mechanism of protective effect of CBLB502 on IR-induced intestinal injury, mice were given CBLB502 and irradiated with different doses at different times. The survival rate, body weight, hemogram and histopathology of the mice were analyzed. The results showed that CBLB502 before IR can reduce intestinal injury induced by IR. RNA-seq analysis showed that different doses and different time of IR induced different damage mechanisms to promote gene regulation patterns. In addition, CBLB502 exerts its protective effect on IR-induced intestinal injury mainly through biological processes such as immune response. Notably, CBLB502 protected against intestinal injury only after IR, and might play a protective role by reversing the regulation of IR-induced genes. Therefore, this paper basically describes the mechanism of IR-induced intestinal injury and the potential molecular protective mechanism of CBLB502, which provides a basis for further research on functional genes and molecular mechanisms that mediate protection against IR-induced injury in the future.

2023-11-10 | GSE246176 | GEO

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