Baicalin attenuates diet induced nonalcoholic steatohepatitis by inhibiting inflammation and oxidative stress via suppressing JNK signaling pathways

Zhong, Xueqing; Liu, Hailin

doi:10.1016/j.biopha.2017.12.026

Cited by 44 publications

(30 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…JNK and NF‐κB signalling pathways are involved in the expression of α‐SMA and collagen 7, 8. Protein levels of p‐JNK and NF‐κB were increased in LX‐2 cells activated by TGF‐β1, and this increase was inhibited by FGF21_ADSCs CM treatment but not by Empty_ADSCs CM or 200 pg/mL FGF21 (Figure 2C,D).…”

Section: Resultsmentioning

confidence: 95%

“…JNK and NF-κB signalling pathways are involved in the expression of α-SMA and collagen. 7,8 Protein levels of p-JNK and NF-κB were increased in LX-2 cells activated by TGF-β1, and this increase was inhibited by FGF21_ADSCs CM treatment but not by Empty_ADSCs CM or 200 pg/ mL FGF21 ( Figure 2C,D). Similarly, p-JNK and NF-κB protein levels were increased in the liver tissues of the TAA-induced fibrotic group, and these levels were decreased by Empty_ADSCs transplantation and further decreased by FGF21_ADSCs transplantation (Figure S3A,B).…”

Section: Regulation Of Jnk and Smad2/3 Signalling By Fgf21_adscsmentioning

confidence: 97%

See 1 more Smart Citation

Effects of FGF21‐secreting adipose‐derived stem cells in thioacetamide‐induced hepatic fibrosis

Kang

Seo

Park

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

Mesenchymal stem cells (MSCs) have been investigated to treat liver diseases, but the efficiency of MSCs to treat chronic liver diseases is conflicting. FGF21 can reduce inflammation and fibrosis. We established FGF21‐secreting adipose derived stem cells (FGF21_ADSCs) to enhance the effects of ADSCs and transplanted them into thioacetamide (TAA)‐induced liver fibrosis mice via the tail vein. Transplantation of FGF21_ADSCs significantly improved liver fibrosis by decreasing serum hyaluronic acid and reducing the expression of fibrosis‐related factors such as α‐smooth muscle actin (α‐SMA), collagen and tissue inhibitor of metalloproteinase‐1 (TIMP‐1) compared with the Empty_ADSCs by inhibition of p‐JNK, NF‐κB and p‐Smad2/3 signalling. α‐lactoalbumin (LA) and lactotransferrin (LTF), secretory factors produced from FGF21_ADSCs inhibited TGF‐β1‐induced expression of α‐SMA and collagen in LX‐2 cells. These results suggest that transplantation of FGF21_ADSCs inhibited liver fibrosis more effectively than Empty_ADSCs, possibly via secretion of α‐LA and LTF.

show abstract

Section: Resultsmentioning

confidence: 95%

Section: Regulation Of Jnk and Smad2/3 Signalling By Fgf21_adscsmentioning

confidence: 97%

Effects of FGF21‐secreting adipose‐derived stem cells in thioacetamide‐induced hepatic fibrosis

Kang

Seo

Park

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Besides, Wu et al proved that BAI alleviated atherosclerosis through attenuating inflammatory response and oxidative stress via repressing p38MAPK pathway (Wu et al, ). Moreover, Zhong et al revealed that BAI ameliorated nonalcoholic steatohepatitis through suppressing oxidative stress and inflammation via inhibiting JNK pathway (Zhong & Liu, ). In addition, miR‐145 was also reported to participate in the regulation of various diseases through regulating JNK and p38MAPK pathways.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Baicalin relieves TNF‐α‐evoked injury in human aortic endothelial cells by up‐regulation of miR‐145

Liu

et al. 2019

Phytotherapy Research

View full text Add to dashboard Cite

Hypertension is recognized to be associated with low‐grade inflammation. Baicalin (BAI) is reported to possess various pharmacological including anti‐inflammatory activities. This research explored the molecular mechanism by which BAI functions in human aortic endothelial cells (HAECs). HAECs were pretreated with BAI. Cell viability, apoptosis, and expressions of crucial proteins were respectively evaluated using cell counting kit‐8 assay, flow cytometry, and western blot. Productions of cytokines were respectively assessed employing quantitative real‐time polymerase chain reaction and enzyme‐linked immunosorbent assay. Cell transfection was utilized to alter miR‐145 expression. The expressions of proteins participated in JNK and p38MAPK pathways were analyzed utilizing western blot. TNF‐α inducement successfully evoked inflammatory injury in HAECs, exhibiting as prominently suppressed viability, while facilitated apoptosis and productions of cytokines. However, BAI pretreatment significantly ameliorated TNF‐α‐triggered inflammatory injuries. Besides, miR‐145 expression was markedly inhibited by TNF‐α inducement, while notably elevated by BAI pretreatment. Although miR‐145 overexpression had no significant influence on apoptosis, miR‐145 silence observably reversed BAI pretreatment‐evoked protective influences on TNF‐α‐induced HAECs, as well as the inhibited impacts on the levels of key proteins involved in JNK and p38MAPK pathways. This investigation illustrated that BAI relieved TNF‐α‐triggered injuries through upregulating miR‐145 via suppressing JNK and p38MAPK pathways.

show abstract

“…The highest reported dose of baicalin at 400 mg/kg/d was safe without significant side effects and significantly reduced obesity and fatty liver disease (Xi et al, 2015). Moreover, baicalin reduced NASH by inhibiting lipid metabolism, inflammation, and fibrosis in mice (Zhang et al, 2018) and reduced diet-induced NASH by inhibiting the activation of the JNK signaling pathway (Zhong and Liu, 2018). Baicalin was effectively used to treat abnormal blood sugar and blood lipid metabolism caused by a long-term highfat diet by adjusting the abundance of the microbiota and changing the production of a variety of SCFAs (Ju et al, 2019).…”

Section: Prevention and Treatment Strategiesmentioning

confidence: 97%

Mechanism and Basis of Traditional Chinese Medicine Against Obesity: Prevention and Treatment Strategies

et al. 2021

View full text Add to dashboard Cite

In the last few decades, the incidences of obesity and related metabolic disorders worldwide have increased dramatically. Major pathophysiology of obesity is termed “lipotoxicity” in modern western medicine (MWM) or “dampness-heat” in traditional Chinese medicine (TCM). “Dampness-heat” is a very common and critically important syndrome to guild clinical treatment in TCM. However, the pathogenesis of obesity in TCM is not fully clarified, especially by MWM theories compared to TCM. In this review, the mechanism underlying the action of TCM in the treatment of obesity and related metabolic disorders was thoroughly discussed, and prevention and treatment strategies were proposed accordingly. Hypoxia and inflammation caused by lipotoxicity exist in obesity and are key pathophysiological characteristics of “dampness-heat” syndrome in TCM. “Dampness-heat” is prevalent in chronic low-grade systemic inflammation, prone to insulin resistance (IR), and causes variant metabolic disorders. In particular, the MWM theories of hypoxia and inflammation were applied to explain the “dampness-heat” syndrome of TCM, and we summarized and proposed the pathological path of obesity: lipotoxicity, hypoxia or chronic low-grade inflammation, IR, and metabolic disorders. This provides significant enrichment to the scientific connotation of TCM theories and promotes the modernization of TCM.

show abstract

Baicalin attenuates diet induced nonalcoholic steatohepatitis by inhibiting inflammation and oxidative stress via suppressing JNK signaling pathways

Cited by 44 publications

References 52 publications

Effects of FGF21‐secreting adipose‐derived stem cells in thioacetamide‐induced hepatic fibrosis

Effects of FGF21‐secreting adipose‐derived stem cells in thioacetamide‐induced hepatic fibrosis

Retracted: Baicalin relieves TNF‐α‐evoked injury in human aortic endothelial cells by up‐regulation of miR‐145

Mechanism and Basis of Traditional Chinese Medicine Against Obesity: Prevention and Treatment Strategies

Contact Info

Product

Resources

About