Kaempferol protects mice from d-GalN/LPS-induced acute liver failure by regulating the ER stress-Grp78-CHOP signaling pathway

Wang, Huijuan; Chen, Liyan; Zhang, Xiangying; Xu, Lin; Xie, Bangxiang; Shi, Hang; Duan, Zhongping; Zhang, Huanhu; Ren, Feng

doi:10.1016/j.biopha.2018.12.105

Cited by 74 publications

(56 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…58) Similarly, catechin, gallic acid, rutin and quercetin also reduce inflammatory marker in this model. [58][59][60] Moreover, kaempferol also inhibits hepatocyte apoptosis in d-GalN/LPS-induced acute liver failure mice 61) while tannic acid reduces NF-κB expression in LPS-induced BV2 microglial cells. 62) Furthermore, polyphenol extract also showed anti-inflamatory effect by reducing plasma LPS and IL-6 levels in human volunteers.…”

Section: Discussionmentioning

confidence: 99%

<i>Spirogyra neglecta</i> Aqueous Extract Attenuates LPS-Induced Renal Inflammation

Ontawong

Srimaroeng

Boonphang

et al. 2019

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Spirogyra neglecta (SN), commonly named "Tao" in Thai, is a genus of filamentous green macroalgae. SN contains polyphenols such as isoquercetin, catechin, hydroquinone and kaempferol. These constituents exhibit beneficial effects including anti-oxidant, anti-gastric ulcer, anti-hyperglycaemia and anti-hyperlipidaemia in both in vitro and in vivo models. Whether SN extract (SNE) has an anti-inflammatory effect in vivo remains unclear. This study examined the effect of SNE on renal function and renal organic transport in lipopolysaccharide (LPS)-induced renal inflammation in rats. Rats were randomised and divided into normal saline (NS), NS supplemented with 1000 mg/kg body weight (BW) of SNE (NS SNE), intraperitoneally injected with 12 mg/kg BW of LPS and LPS treated with 1000 mg/kg BW of SNE (LPS SNE). Biochemical parameters in serum and urine, lipid peroxidation concentration, kidney function and renal organic anion and cation transports were determined. LPS-injected rats developed renal injury and inflammation by increasing urine microalbumin, total malondialdehyde (MDA) and inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-1β protein expression, respectively. In addition, uptake of renal organic anion, [ 3 H]-oestrone sulphate (ES), was reduced in LPS-injected rats together with increased expression of organic anion transporter 3 (Oat3). However, the renal injury and inflammation, as well as impaired Oat3 function and protein expression, were restored in LPS SNE rats. Accordingly, SNE could be developed as nutraceutical product to prevent inflammation-induced nephrotoxicity.

show abstract

Section: Discussionmentioning

confidence: 99%

<i>Spirogyra neglecta</i> Aqueous Extract Attenuates LPS-Induced Renal Inflammation

Ontawong

Srimaroeng

Boonphang

et al. 2019

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…was also con rmed by others' studies to have anti-oxidative, anti-in ammatory and anti-ER stress properties in response to acetaminophen-induced liver failure in mice [27,28]. Keampferol and tanshinone IIA were supported against liver failure by literature [29,30]. No evidence about other ingredients against liver failure was reported.…”

Section: Discussionmentioning

confidence: 83%

Uncovering bioactive compounds and potential mechanisms of Jieduan-Niwan Formula against liver failure

Ma¹,

Zhang²,

Gao³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Liver failure is considered as the inability of the liver to perform its normal synthetic and metabolic function. Our previous data showed that Jieduan-Niwan formula (JDNW) induced liver failure, while its underlying mechanism remains unknown. Methods In the present study, we performed a network pharmacology to analyze the bioactive ingredients and related targets. Compound and target data of JDNW formula were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database (TCMSP), and targets related to liver diseases were obtained from DisGeNET database. Information of protein protein interaction were retrieved from STRING database. Network construction and degree calculation were used Cytoscape software. Metascape web-server was used for GO and KEGG pathway enrichment. A microarray data series (GSE72081) was obtained from Gene Expression Omnibus database and analyzed using R project and Connectivity Map. Ledock was used for molecular docking. Results A total of 114 unduplicated active ingredients were identified after ADME screening. After construction of a target-liver disease network, 28 targets were identified for anti-liver failure effect. These targets were significantly enriched in fluid shear stress and atherosclerosis, pathways in cancer, IL-17 signaling pathway, HIF-1 signaling pathway, insulin resistance, toxoplasmosis, prostate cancer, microRNAs in cancer, NF-kappa B signaling pathway, Chemical carcinogenesis, VEGF signaling pathway and complement and coagulation cascades pathways. After analyzing a public microarray data of quercetin, we found biological action of some NFκB inhibitors was similar to quercetin. Molecular docking study showed that quercetin possessed a capability to bind on IKKβ and inhibited NFκB activation. Conclusions JDNW formula treated liver failure via multiple targets and multiple pathways, including NFκB signal. Quercetin was identified as a key bioactive ingredient of JDNW formula and its anti-liver failure effect may involve in NFκB inhibition.

show abstract

“…Particularly, dietary choices that modify the PI3K/AKT/PTEN signaling pathway may prevent FLD or decrease the rate of disease progression (60). Certain plants and fruits are promising targets (61)(62)(63)(64)(65)(66)(67).…”

Section: Diet and Hepatocyte Protectionmentioning

confidence: 99%

Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review)

et al. 2020

View full text Add to dashboard Cite

Fatty liver disease (FLD) is characterized by accumulation of excess fat in the liver. The underlying molecular mechanism associated with the progression of the disease has been in elusive. Hepatocellular demise due to increased oxidative stress resulting in an inflammatory response may be a key feature in FLD. Recent advances in molecular biology have led to an improved understanding of the molecular pathogenesis, suggesting a critical association between the PI3K/AKT/PTEN signaling pathway and FLD. In particular, PTEN has been associated with regulating the pathogenesis of hepatocyte degeneration. Given the function of mitochondria in reactive oxygen species (ROS) generation and the initiation of oxidative stress, the mitochondrial antioxidant network is of interest. It is vital to balance the activity of intracellular key molecules to maintain a healthy liver. Consequently, onset of FLD may be delayed using dietary protective agents that alter PTEN signaling and reduce ROS levels. The advancement of research on dietary regulation with a focus on modulatory roles in ROS generation and PTEN associated signaling is summarized in the current study, supporting further preventive and therapeutic exploration.

show abstract

Kaempferol protects mice from d-GalN/LPS-induced acute liver failure by regulating the ER stress-Grp78-CHOP signaling pathway

Cited by 74 publications

References 31 publications

<i>Spirogyra neglecta</i> Aqueous Extract Attenuates LPS-Induced Renal Inflammation

<i>Spirogyra neglecta</i> Aqueous Extract Attenuates LPS-Induced Renal Inflammation

Uncovering bioactive compounds and potential mechanisms of Jieduan-Niwan Formula against liver failure

Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review)

Contact Info

Product

Resources

About