Huangqin decoction mitigates hepatic inflammation in high-fat diet-challenged rats by inhibiting TLR4/NF-κB/NLRP3 pathway

Yan, Baofei; Wang, Yun; Wang, Wenbo; Ding, Xiaoqing; Wei, Bin; Liu, Shengjin; Fu, Tingming; Chen, Ling; Zhang, Jing-Zheng; Liu, Jia; Zheng, Xiaoya

doi:10.1016/j.jep.2022.115999

Cited by 15 publications

(16 citation statements)

References 42 publications

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“…Oxidative stress and inflammation, secondary to hepatosteatosis, are the main risk factors promoting the exacerbation of NAFLD to NASH. 24 In the present study, HFD-induced NAFLD mice livers showed increased staining intensity of IL-6 and TNF-α, as well as infiltration of F4/80-and CD68-positive macrophages, further evidenced by the elevated levels of serum IL-6, IL-1β, and TNF-α. In parallel, FFA remarkably aggrandized the secretion of IL-6, IL-1β, and TNF-α in HepG2 cells.…”

Section: ■ Discussionsupporting

confidence: 61%

“…Abnormal fasting insulin levels, OGTT, and HOMA-IR were observed in HFD-induced mice, indicating the onset of insulin resistance, which was further supported by the compromised glucose uptake in FFA-stimulated HepG2 cells. Oxidative stress and inflammation, secondary to hepatosteatosis, are the main risk factors promoting the exacerbation of NAFLD to NASH . In the present study, HFD-induced NAFLD mice livers showed increased staining intensity of IL-6 and TNF-α, as well as infiltration of F4/80- and CD68-positive macrophages, further evidenced by the elevated levels of serum IL-6, IL-1β, and TNF-α.…”

Section: Discussionsupporting

confidence: 59%

“…Similarly, HepG2 cells were also fixed and stained with Oil red O. Immunofluorescence examination was performed on the aforementioned sections as we described previously. 24 The images were acquired using an LSM 700 confocal laser microscope and quantified using Image-Pro Plus 6.0 software (Media Cybernetics, Maryland, USA).…”

Section: ■ Conclusionmentioning

confidence: 99%

“…Immunoblot analysis was performed referring to our previous work. 24 Specific primary antibodies against CD36, FAS, MGL, FATP2, SREBP-1, and β-actin were utilized at a 1000-fold dilution. Protein bands were visualized and semiquantified using the Azure Biosystems C600 (Azure Biosystems Inc., CA, USA) and ImageJ software (NIH, Bethesda, MD, USA), respectively.…”

Section: ■ Conclusionmentioning

confidence: 99%

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Liposome-Based Silibinin for Mitigating Nonalcoholic Fatty Liver Disease: Dual Effects via Parenteral and Intestinal Routes

Yan,

Zheng,

Wang

et al. 2023

ACS Pharmacol. Transl. Sci.

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Section: ■ Discussionsupporting

confidence: 61%

Section: Discussionsupporting

confidence: 59%

Section: ■ Conclusionmentioning

confidence: 99%

Section: ■ Conclusionmentioning

confidence: 99%

See 2 more Smart Citations

Liposome-Based Silibinin for Mitigating Nonalcoholic Fatty Liver Disease: Dual Effects via Parenteral and Intestinal Routes

Yan,

Zheng,

Wang

et al. 2023

ACS Pharmacol. Transl. Sci.

Self Cite

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“…Ameliorating the low‐grade inflammation companied with obesity by ω‐3 PUFA benefits obesity via modulating pro‐inflammatory mediators secretion (Khatib et al, 2016). In acute and chronic inflammation, NFκB is considered a critical factor in regulating the immune response to infection (Yan et al, 2023). Activation of NFκB can induce the expression of TNF‐α, IL‐1β, and IL‐6, increasing the expression of pro‐inflammatory molecules (Hwang et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Effects of fatty acid‐ethanol amine (FA‐EA) derivatives on lipid accumulation and inflammation

Huang

et al. 2023

Lipids

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This study aimed to investigate the effect of fatty acid-ethanol amine (FA-EA) derivatives (L1-L10) on the mitigation of intracellular lipid accumulation and downregulation of pro-inflammatory cytokines in vitro. First, the series of FA-EA derivatives were synthesized and characterized. Then, their cytotoxic, intracellular lipid accumulation and inhibition of pro-inflammatory cytokines were evaluated. The oil red O staining experiment showed that the tested compounds L4, L6, L8, L9, and L10 could reduce intracellular lipid accumulation induced by palmitic acid (PA). Moreover, ω-3/ω-6 PUFA-EA derivatives showed inhibitory effect on the production of pro-inflammatory cytokines in lipopolysaccharide (LPS) -stimulated RAW 264.7 cells. ω-3/ω-6 PUFA-EA derivatives at a concentrations of 10 μM could significantly decrease mRNA levels of IL-6, IL-1β, and TNF-α, inhibit NO production, and alleviate the protein expression of IL-1β in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. These data suggest that ω-3 PUFA-EA derivatives can be beneficial for further pharmaceutical development to treat chronic low-grade inflammation diseases such as obesity.

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Huang Qin decoction increases SLC6A4 expression and blocks the NFκB-mediated NLRP3/Caspase1/GSDMD pathway to disrupt colitis-associated carcinogenesis

Tao,

Wang,

et al. 2024

Funct Integr Genomics

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Huang Qin decoction (HQD) is a traditional Chinese medicine formula for treating colitis, but the effects and molecular mechanism of action of HQD in colitis-associated carcinogenesis (CAC) are still unclear. Therefore, we aimed to determine the beneficial effects of HQD on CAC in mice and to reveal the underlying mechanism involved. AOM/DSS was used to induce CAC in mice, and the effects of HQD on tumorigenesis in mice were examined (with mesalazine serving as a positive control). Mesalazine or HQD treatment alleviated body weight loss and decreased the disease activity index in mice induced by AOM/DSS. Mesalazine or HQD treatment also suppressed the shortening of colon tissue length, the number of tumors, and the infiltration of inflammatory cells. The genes targeted by HQD were predicted and verified, followed by knockout experiments. Elevated SLC6A4 and inhibited serotonin production and inflammation were observed in HQD-treated mice. HQD inhibited the NFκB and NLRP3/caspase1/GSDMD pathways. The therapeutic effect of HQD was diminished in SLC6A4-deficient AOM/DSS mice. Additionally, the downregulation of SLC6A4 mitigated the inhibitory effect of HQD-containing serum on MODE-K cell pyroptosis. Our findings suggest that SLC6A4 is a pivotal regulator of HQD-alleviated CAC via its modulation of the NLRP3/caspase1/GSDMD pathway.

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Huangqin decoction mitigates hepatic inflammation in high-fat diet-challenged rats by inhibiting TLR4/NF-κB/NLRP3 pathway

Cited by 15 publications

References 42 publications

Liposome-Based Silibinin for Mitigating Nonalcoholic Fatty Liver Disease: Dual Effects via Parenteral and Intestinal Routes

Liposome-Based Silibinin for Mitigating Nonalcoholic Fatty Liver Disease: Dual Effects via Parenteral and Intestinal Routes

Effects of fatty acid‐ethanol amine (FA‐EA) derivatives on lipid accumulation and inflammation

Huang Qin decoction increases SLC6A4 expression and blocks the NFκB-mediated NLRP3/Caspase1/GSDMD pathway to disrupt colitis-associated carcinogenesis

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