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Yishen Jiangzhuo decoction attenuates cisplatin-induced acute kidney injury by inhibiting inflammation, oxidative stress, and apoptosis through the TNF signal pathway

ABSTRACT: Yishen Jiangzhuo decoction attenuates cisplatin-induced acute kidney injury by inhibiting inflammation, oxidative stress, and apoptosis through the TNF signal pathway

PROVIDER: PRJNA1093396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28496645_1.fastq.gz	Fastqsanger.gz
	SRR28496645_2.fastq.gz	Fastqsanger.gz
	SRR28496646_1.fastq.gz	Fastqsanger.gz
	SRR28496646_2.fastq.gz	Fastqsanger.gz
	SRR28496647_1.fastq.gz	Fastqsanger.gz

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Yishen Jiangzhuo decoction attenuates cisplatin-induced acute kidney injury by inhibiting inflammation, oxidative stress, and apoptosis through the TNF signal pathway

Project description:We aimed to investigate the therapeutic effects and mechanisms of Yishen Jiangzhuo decoction (YSJZD) in a mouse model of cisplatin-induced acute kidney injury (AKI). The mice were divided into the NC, cisplatin, and cisplatin + YSJZD groups. A concentration-dependent effect of YSJZD on cisplatin-induced AKI was observed, and the optimal concentration for intervention was calculated. Changes in blood urea nitrogen and serum creatinine levels combined with hematoxylin & eosin and periodic acid-Schiff staining, and transmission electron microscopy observations indicated that YSJZD enhanced renal function, reduced pathological injury, and protected renal tubular epithelial cells in cisplatin-induced AKI mice. The results of the transcriptomic and enrichment analyses showed that the mechanisms of YSJZD may be associated with inflammation, oxidation, apoptosis, and the TNF signal pathway. Immunofluorescence, oxidative stress index, terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and western blotting (WB) revealed that YSJZD downregulated apoptosis in the renal tissues of AKI mice, and further decreased the expression levels of p-p65, p-p38 MAPK, tumor necrosis factor -α, cleaved-caspase-3, and malondialdehyde, while increasing the levels of SIRT3, GSH, and SOD. Overall, the results showed that YSJZD could effectively abrogate cisplatin-induced AKI in mice through mechanisms primarily related to its anti-inflammatory, antioxidative, and antiapoptotic effects by inhibited the TNF signal pathway. YSJZD warrants further investigation as a clinical empirical prescription.

2024-04-06 | GSE262792 | GEO

Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

Project description:In this study, cisplatin activated cGAS-STING signal pathway and deficiency of STING attenuated cisplatin-induced cardiotoxicity in vivo and in vitro. Mechanistically, STING-TNF-α-AP-1 axis contributed to cisplatin-induced cardiotoxicity by triggering cardiomyocyte apoptosis.

2021-08-12 | GSE181749 | GEO

Effects of Huatan Jiangzhuo Decoction and Poria cocos - Alismatis Rhizoma on gene expression in liver of rats with hyprelipidemia

Project description:Huatan Jiangzhuo Decoction, a traditional Chinese medicine composition, has been used to treat patients with hyperlipidemia (HLP). To investigate the therapeutic mechanism of Huatan Jiangzhuo decoction(HTJZD) and Poria cocos (PC) - Alismatis Rhizoma (AR) on gene expression in liver of rats with HLP, this study performed gene expression profiling analysis using data obtained from RNA-seq technology. It’s predicted that the potential role of regulating the expression of differentially expressed genes in the treatment of HLP by HTJZD and PC-AR separately.

2023-06-30 | GSE212771 | GEO

Yishen Jiangzhuo decoction attenuates cisplatin‑induced acute kidney injury by inhibiting inflammation, oxidative stress and apoptosis through the TNF signal pathway.

Project description:The present study aimed to investigate the therapeutic effects and mechanisms of Yishen Jiangzhuo decoction (YSJZD) in a mouse model of cisplatin-induced acute kidney injury (AKI). The mice were divided into the NC, cisplatin and cisplatin + YSJZD groups. A concentration-dependent effect of YSJZD on cisplatin-induced AKI was observed and the optimal concentration for intervention was calculated. Changes in blood urea nitrogen and serum creatinine levels combined with hematoxylin and eosin and periodic acid-Schiff staining and transmission electron microscopy observations indicated that YSJZD enhanced renal function, reduced pathological injury and protected renal tubular epithelial cells in cisplatin-induced AKI mice. The results of the transcriptomic and enrichment analyses showed that the mechanisms of YSJZD may be associated with inflammation, oxidation, apoptosis and the TNF signal pathway. Immunofluorescence, oxidative stress index, terminal deoxynucleotidyl transferase dUTP nick end labeling assay and western blotting revealed that YSJZD downregulated apoptosis in the renal tissues of AKI mice and further decreased the expression levels of p-p65, p-p38 MAPK, TNF-α, cleaved-caspase-3 and malondialdehyde, while increasing the levels of NAD-dependent protein deacetylase sirtuin-3, glutathione and superoxide dismutase. Overall, the results showed that YSJZD could effectively abrogate cisplatin-induced AKI in mice through mechanisms primarily related to its anti-inflammatory, antioxidative and antiapoptotic effects by inhibited the TNF signal pathway. YSJZD warrants further investigation as a clinical empirical prescription.

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Plant microRNA profiling of Honeysuckle and Honeysuckle Decoction

Project description:Influenza A viruses (IAVs), particularly H1N1, H5N1 and H7N9, pose a substantial threat to public health worldwide. Here, we report that MIR2911, a honeysuckle (HS)-encoded atypical microRNA, directly targets IAVs with a broad spectrum. MIR2911 is highly stable in HS decoction, and continuous drinking or gavage feeding of HS decoction leads to a significant elevation of the MIR2911 level in mouse peripheral blood and lung. Bioinformatics prediction and a luciferase reporter assay showed that MIR2911 could target various IAVs, including H1N1, H5N1 and H7N9. Synthetic MIR2911 significantly inhibited H1N1-encoded PB2 and NS1 protein expression but did not affect mutants in which the MIR2911-binding nucleotide sequences were altered. Synthetic MIR2911, extracted RNA from HS decoction and HS decoction all significantly inhibited H1N1 viral replication and improved viral infection-induced mouse weight loss but did not affect infection with a mutant virus in which the MIR2911-binding nucleotide sequences of PB2 and NS1 were altered. Importantly, the inhibitory effect of HS decoction on viral replication was abolished by an anti-MIR2911 antagomir, indicating that the physiological concentration of MIR2911 in HS decoction could directly and sufficiently suppress H1N1 viral replication. MIR2911 also inhibited H5N1 and H7N9 viral replication in vitro and in vivo. Strikingly, administration of MIR2911 or HS decoction both dramatically reduced mouse mortality caused by H5N1 infection. Our results demonstrate that MIR2911 is the first active component identified in Traditional Chinese Medicine to directly target various IAVs and may represent a novel type of natural product that effectively suppresses viral infection. Screening and profiling of known plant microRNA in HS and HS decoction

2014-10-22 | E-GEOD-55268 | biostudies-arrayexpress

RNA-seq revealed the protective effect of Huangqi Guizhi Wuwu Decoction against cisplatin induced PC12 cell injury

Project description:Chemotherapy-induced peripheral neuropathy (CIPN) not only impacts chemotherapy regimens but also causes intolerable and long-lasting effects on cancer patients. Currently, duloxetine is the only drug used to treat CIPN. However, the clinical use of this drug still faces several challenges. Therefore, we focused on traditional Chinese medicine (TCM) to find an effective and safe alternative medicine. Huangqi Guizhi Wuwu Decoction (HGWD) is a traditional Chinese medicine that has been clinically used for treating nerve pain for thousands of years. This study aimed to investigate the neuroprotective effect of HGWD on cisplatin-induced injury in PC12 cells and to elucidate its potential mechanism of action.

2025-06-07 | GSE269389 | GEO

Yangyinqingfei Decoction attenuates PM2.5-induced lung injury by enhancing arachidonic acid metabolism

Project description:Yangyinqingfei Decoction (YYQFD), a traditional Chinese prescription, is well known in the treatment of diphtheria and lung-related diseases in clinic. However, the underlying mechanism how to treat lung-related diseases remains unclear. In the present study, the intervention effect of YYQFD on PM2.5-induced lung injury mice and its potential mechanism were investigated by metabolomics and proteomic techniques. The results showed that YYQFD could significantly improve pulmonary functions, relieve lung injury, as well as reduce IL-6, TNF-α and MDA, and increase SOD levels in serum and BALF of PM2.5-induced lung injury mice. Furthermore, the protein-metabolite joint analysis presented that YYQFD regulated the pathways of arachidonic acid metabolism, linoleic acid metabolism, and biosynthesis of unsaturated fatty acids with significantly down-regulating arachidonic acid, 20-HETE, prostaglandin E2, lecithin, linoleic acid, α-linolenic acid, eicosatetraenoic acid, and γ-linolenic acid, and up-regulating PTGES2, GPX2 and CBR3 protein expressions in lung tissue. A regulatory metabolic network map was further constructed, which provide us a better understanding about the role of YYQFD on PM2.5-induced lung injury mice and new insight into YYQFD application for the treatment of lung-related diseases.

2022-12-22 | PXD037163 | Pride

A novel lncRNA XLOC_032768 rescues cisplatin-induced apoptosis of renal tubular cells and acute kidney injury by repressing TNF-α expression in trans-manner [mouse]

Project description:The cellular and molecular mechanisms by which cisplatin induces nephrotoxicity have been investigated extensively. However, the role of long non-coding RNAs (lncRNAs) in cisplatin-induced nephrotoxicity has not been received much attention. Here, we explore the functions and underlying mechanisms of a novel lncRNA XLOC_032768 in cisplatin-induced nephrotoxicity. Cisplatin treatment resulted in the apoptosis of renal epithelial cells in a mouse model and human renal proximal tubular epithelial cells (HK-2). By performing differentially expressed genes (DEGs) of the transcriptome data, we found the expression of lncRNA XLOC_032768 was significantly repressed by cisplatin treatment, which was also validated by RT-qPCR experiment of in vivo and in vitro model. Overexpression of lncRNA XLOC_032768 significantly inhibited the cisplatin-induced apoptosis of HK-2 and the expression of biomarkers for cisplatin-induced nephrotoxicity. Results from XLOC_032768 overexpression experiment revealed that XLOC_032768 target the tumor necrosis factor (TNF)-α in trans in HK-2 cells and mouse exposed to cisplatin. The administration of lncRNA XLOC_032768 attenuated renal dysfunction, morphological damage, and renal tubular cell injury, which was accompanied by TNF-α preservation, in a mouse model of cisplatin nephrotoxicity. These data indicate that XLOC_032768 suppressed cisplatin-induced apoptosis of tubular epithelial cells and acute kidney injury via a TNF mechanism. LncRNA XLOC_032768 would be a novel agent to reduce cisplatin-induced nephrotoxicity.

2021-07-27 | GSE142137 | GEO

A novel lncRNA XLOC_032768 rescues cisplatin-induced apoptosis of renal tubular cells and acute kidney injury by repressing TNF-α expression in trans-manner [human]

2021-07-27 | GSE142134 | GEO

Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

Project description:Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

| PRJNA753284 | ENA

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