Imidacloprid-induced liver fibrosis in quails via activation of the TGF-β1/Smad pathway

Lv, Yueying; Bing, Qizheng; Lv, Zhanjun; Xue, Jianming; Li, Siyu; Han, Bing; Yang, Qingyue; Wang, Xiaoqiao; Zhang, Zhigang

doi:10.1016/j.scitotenv.2019.135915

Cited by 79 publications

(39 citation statements)

References 63 publications

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“…Recombinant human Trx can inhibit the production and release of pro-inflammatory mediators at the site of inflammation and inhibit ICD (25). Furthermore, IL-1β produced by inflammatory cells stimulates renal epithelial cells to produce downstream inflammatory cytokines, TNF-α and IL-6 (26). Similarly, the inhibitory effect of Trx on inflammatory cytokines (IL-1β and TNF-α) was observed in the serum of AKI mice in the present study.…”

Section: Discussionsupporting

confidence: 73%

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Wang

Zhang

Lu³

2021

Exp Ther Med

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Acute kidney injury (AKI) is a serious disease with rapid onset and a high mortality rate. It is therefore particularly important to identify a suitable method for treating AKI. Thioredoxin (Trx) is a potent anti-inflammatory and anti-oxidant protein that is prevalent in living organisms. The aim of the present study was to facilitate the clinical treatment of AKI via the study of Trx. Lipopolysaccharide (LPS) was used to construct an AKI model in mice and the mice were pre-treated with Trx to examine its effect on AKI. In addition, human renal tubular epithelial HK-2 cells were cultured and stimulated with Trx to examine its effect on inflammation, levels of oxidative stress and apoptosis in the HK-2 cells. The NF-κB signaling pathway is a classical inflammation-related pathway and the mechanism of Trx was investigated by evaluating the association between Trx and the NF-κB signaling pathway. Trx treatment reduced LPS-induced levels of inflammation, oxidative stress and apoptosis in the HK-2 cells. The activity of NF-κB signaling pathway was increased in LPS-induced HK-2 cells, while Trx treatment effectively reduced NF-κB signaling pathway activity. In addition, Trx treatment significantly reduced LPS-induced mouse AKI in vivo, which was characterized by a decrease in inflammatory factors in mouse serum, a decrease in AKI-associated molecules in mouse urine and a decrease in oxidative stress levels in mouse kidney tissue samples. Trx treatment reduced inflammation, levels of oxidative stress and apoptosis in HK-2 cells by inhibiting the NF-κB signaling pathway, thereby alleviating LPS-induced mouse AKI.

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Section: Discussionsupporting

confidence: 73%

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Wang

Zhang

Lu³

2021

Exp Ther Med

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“…6). In the future study, it will be also needed to measure fibronectin 1 and col1a1 protein expression because these proteins are fibrosis markers (32).…”

Section: Discussionmentioning

confidence: 99%

Effects of renalase deficiency on liver fibrosis markers in a nonalcoholic steatohepatitis mouse model

et al. 2021

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Progression of nonalcoholic steatohepatitis (NASH) is attributed to several factors, including inflammation and oxidative stress. In recent years, renalase has been reported to suppress oxidative stress, apoptosis and inflammation. A number of studies have suggested that renalase may be associated with protecting the liver from injury. The present study aimed to clarify the effects of renalase knockout (KO) in mice with NASH that were induced with a choline-deficient high-fat diet (CDAHFD) supplemented with 0.1% methionine. Wild type (WT) and KO mice (6-week-old) were fed a normal diet (ND) or CDAHFD for 6 weeks, followed by analysis of the blood liver function markers and liver tissues. CDAHFD intake was revealed to increase blood hepatic function markers, lipid accumulation and oxidative stress compared with ND, but no significant differences were observed between the WT and KO mice. However, in the KO-CDAHFD group, the Adgre1 and Tgfb1 mRNA levels were significantly higher, and α-SMA expression was significantly lower compared with the WT-CDAHFD group. Furthermore, the Gclc mRNA and phosphorylated protein kinase B (Akt) levels were significantly lower in the KO-ND group compared with the WT-ND group. The results of the current study indicated that as NASH progressed in the absence of renalase, oxidative stress, macrophage infiltration and TGF-β expression were enhanced, while α-SMA expression in NASH may be partly suppressed due to the decreased phosphorylation of Akt level.

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“…When the body encounters stresses, Nrf2 is released into the nucleus, binding to the ARE sequence of the downstream target genes to promote the expression of phase II detoxification enzymes, including NQO1 and HO-1, which can alleviate mitochondrial dysfunction and resist excessive oxidative stress [ 49 ]. Furthermore, inhibition of Nrf2 can not only result in TLR4/NF κ B-mediated proinflammatory response [ 50 ], but also promote fibrosis via the activation of TGF- β 1/Smad pathway [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Huayu Tongluo Recipe Attenuates Renal Oxidative Stress and Inflammation through the Activation of AMPK/Nrf2 Signaling Pathway in Streptozotocin- (STZ-) Induced Diabetic Rats

Guo

Yang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Diabetic nephropathy (DN), a severe microvascular complication of diabetes, is one of the leading causes of end-stage renal disease. Huayu Tongluo Recipe (HTR) has been widely used in the clinical treatment of DN in China, and its efficacy is reliable. This study aimed to explore the renoprotective effect of HTR and the underlying mechanism. Male Sprague-Dawley rats were fed with high sugar and fat diet combined with an intraperitoneal injection of STZ to establish the diabetic model. Rats in each group were respectively given drinking water, HTR, and irbesartan by gavage for 16 weeks. 24-hour urine samples were collected every 4 weeks to detect the content of total protein and 8-OHdG. Blood samples were taken to detect biochemical indicators and inflammatory markers at the end of 16th week. Renal tissue was collected to investigate pathological changes and to detect oxidative stress and inflammatory markers. AMPK/Nrf2 signaling pathway and fibrosis-related proteins were detected by immunohistochemistry, immunofluorescence, real-time PCR, and western blot. 24h urine total protein (24h UTP), serum creatinine (Scr), blood urea nitrogen (BUN), total cholesterol (TC), and triglyceride (TG) were decreased in the rats treated with HTR, while there was no noticeable change of blood glucose. HTR administration decreased malondialdehyde (MDA) content and increased superoxide dismutase (SOD) activity in kidneys, complying with reduced 8-OHdG in the urine. The levels of TNF-α, IL-1β, and MCP1 and the expression of nuclear NFκB were also lower after HTR treatment. Furthermore, HTR alleviated pathological renal injury and reduced the accumulation of extracellular matrix (ECM). Besides, HTR enhanced the AMPK/Nrf2 signaling and increased the expression of HO-1 while it inhibited the Nox4/TGF-β1 signaling in the kidneys of STZ-induced diabetic rats. HTR can inhibit renal oxidative stress and inflammation to reduce ECM accumulation and protect the kidney through activating the AMPK/Nrf2 signaling pathway in DN.

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Imidacloprid-induced liver fibrosis in quails via activation of the TGF-β1/Smad pathway

Cited by 79 publications

References 63 publications

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Effects of renalase deficiency on liver fibrosis markers in a nonalcoholic steatohepatitis mouse model

Huayu Tongluo Recipe Attenuates Renal Oxidative Stress and Inflammation through the Activation of AMPK/Nrf2 Signaling Pathway in Streptozotocin- (STZ-) Induced Diabetic Rats

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