Effect of Rheum palmatum L. on NF-κB signaling pathway of mice with acute liver failure

Zhang, Rongzhen; Qiu, Hua; Wang, Na; Long, Fuli; Mao, Dewen

doi:10.1016/j.apjtm.2015.09.011

Cited by 25 publications

(13 citation statements)

References 31 publications

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“…By modulating mRNAs of the different elements on NF-κB pathway or using NF-κB inhibitors, we proved that JDHY has a potential role to decrease the production of pro-inflammatory cytokines (TNF-α, IL6, and IFN-γ), increase anti-inflammatory cytokines (IL10, IL13), and promote cell survival and proliferation not only in rat model but also on immortalized Kupffer cells. It is noteworthy that Radix curcumae and Rheum officinale , two active gradients of JDHY, were reported to reduce proinflammatory cytokines and reduce inflammation in the serum of ALF mice by blocking NF-κB signal pathways 16,17. Based on our finding and previous reports, we have more confidence that JDHY exerts its clinical effect by targeting NF-κB pathway.…”

Section: Discussionsupporting

confidence: 76%

<p>The underlying mechanisms of Jie-Du-Hua-Yu granule for protecting rat liver failure</p>

Qiu

Mao

Tang

et al. 2019

DDDT

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Objectives Jie-Du-Hua-Yu (JDHY) granule is a combination of six traditional Chinese medicines with known therapeutic effect in treating acute liver failure (ALF). The aim of this study was to investigate the amelioration efficacy of JDHY in lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced ALF in rat and explore the possible molecular mechanism underlying the therapeutic efficacy. Materials and methods The efficacy of JDHY was determined by assessing hepatic pathology and function in LPS and D-GalN challenged Wistar rat. We also evaluated the effect of JDHY on LPS-induced Kupffer cells by measuring inflammatory cytokines and determining the phenotypic function. By means of bioinformatics analysis of liver tissue and validation in Kupffer cells, we identified possible pathways involved in the pharmacologic action of mechanism of JDHY. Results JDHY could attenuate LPS-induced liver injury in rat by inhibiting apoptosis and increasing hepatic activity. In vitro study showed that JDHY could decrease the production of proinflammatory cytokines (tumor necrosis factor-α, IL6, and interferon-γ), increase anti-inflammatory cytokines (IL10, IL13), and promote cell survival and proliferation, possibly due to inhibition of IκB/nuclear factor-κB (NF-κB) signaling pathway and expression of CD14 and CXCL2, which was consistent with the findings from bioinformatics analysis. Conclusion Our results revealed that JDHY protected against LPS-induced liver damage both in vitro and in vivo, by inhibiting the NF-κB-mediated inflammatory pathway, indicating its potential function to treat liver diseases.

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Section: Discussionsupporting

confidence: 76%

<p>The underlying mechanisms of Jie-Du-Hua-Yu granule for protecting rat liver failure</p>

Qiu

Mao

Tang

et al. 2019

DDDT

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“…It also protects against liver damage by inducing CCl 4 that correlates with antioxidant and free radical scavenger effects [ 20 ]. Rheum officinale was found to reduce inflammation in the serum of ALF mice by regulating NF- κ B signaling pathways and the expression of proteins against apoptosis [ 21 ]. Oldenlandia diffusa inhibits inflammation via suppression of caspase-1 activation in mouse peritoneal macrophages [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Herbal Compound “Jiedu Huayu” Reduces Liver Injury in Rats via Regulation of IL‐2, TLR4, and PCNA Expression Levels

Wang

Shi

Zhang

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Aim of the Study. To investigate the preventative effects of Jiedu Huayu (JDHY) on D-galactosamine (D-GalN) and lipopolysaccharide-induced acute liver failure (ALF) and to evaluate the possible mechanisms of action. Materials and Methods. ALF was induced in Wistar rats by administrating D-GalN (900 mg/kg) and lipopolysaccharide (10 μg/kg). After treatment with JDHY granules, the levels of blood alanine aminotransferase, aspartate aminotransferase, total bilirubin, and prothrombin time were determined. Proliferating cell nuclear antigen was detected by immunohistochemistry staining. The expression of interleukin-2 (IL-2) and toll-like receptor 4 (TLR4) was examined by fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot. Results. JDHY treatment dramatically improved liver function and increased survival rates in an ALF model in rats. We observed a decrease in IL-2 and TLR4 expression following treatment with JDHY in liver cells from ALF rats using qRT-PCR and Western blot analysis. Conclusion. We hypothesize that the therapeutic potential of JDHY for treating ALF is due to its modulatory effect on the suppression of inflammation and by promoting hepatocyte regeneration. Our results contribute towards validation of the traditional use of JDHY in the treatment of liver disease.

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“…After staining, 5 different fields under microscope with 200x magnifications were randomly selected from each tissue slides for analysis, and the data were presented by the area percentage of positive staining with blue color, from quantitation using Image Pro Plus 6.0 software (Media Cybernetics Inc, United States). In addition, HE staining was performed to analyze the liver structure according to the protocol described previously [50]. …”

Section: Methodsmentioning

confidence: 99%

Activation of NLRP3 inflammasomes in mouse hepatic stellate cells during Schistosoma J. infection

et al. 2016

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The major pathological changes during Schistosoma J. infection are characterized by granulomatous inflammation in the liver, a cellular immune response to schistosomal egg antigens. The molecular mechanisms initiating or promoting this schistosomal granulomatous inflammation remain poorly understood. In the present study, we first demonstrated that in mice infected with Schistosoma J. for 6 weeks exhibited increased levels of IL-1β in liver, a major product of NLRP3 inflammasomes and collagen deposition around the eosinophilic granuloma with Schistosoma J. eggs, which was substantially attenuated by caspase-1 inhibitor, YVAD. This activation of the NLRP3 inflammasome occurred in hepatic stellate cells (HSCs), as shown by a marked increase in co-localization of IL-1β with HSCs marker, desmin. Using isolated, cultured mouse HSCs, we further explored the mechanisms by which soluble egg antigen (SEA) from Schistosoma J. activates NLRP3 inflammasomes. SEA induced the formation and activation of NLRP3 inflammasomes, which was associated with both redox regulation and lysosomal dysfunction, but not with potassium channel activation. These results suggest that NLRP3 inflammasome activation in HSCs may serve as an early mechanism to turn on the inflammatory response and thereby instigate liver fibrosis during Schistosoma J. infection.

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Effect of Rheum palmatum L. on NF-κB signaling pathway of mice with acute liver failure

Abstract: Through NF-κB signaling pathway, the R. palmatum L. could reduce the content of enzyme of liver function and inflammation factor in the serum of ALF mice, regulate the expression of cell apoptosis-related protein and improve the symptoms of ALF mice.

Cited by 25 publications

References 31 publications

<p>The underlying mechanisms of Jie-Du-Hua-Yu granule for protecting rat liver failure</p>

<p>The underlying mechanisms of Jie-Du-Hua-Yu granule for protecting rat liver failure</p>

Herbal Compound “Jiedu Huayu” Reduces Liver Injury in Rats via Regulation of IL‐2, TLR4, and PCNA Expression Levels

Activation of NLRP3 inflammasomes in mouse hepatic stellate cells during Schistosoma J. infection

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