Pharmacological properties of baicalin on liver diseases: a narrative review

Yang, Jinyu; Li, Min; Zhang, Chengliang; Liu, Dong

doi:10.1007/s43440-021-00227-1

Cited by 61 publications

(38 citation statements)

References 101 publications

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“…Baicalin, a flavonoid glycoside that originates from Scutellaria baicalensis Georgi root tissue, has strong antioxidant reaction activity, and has been known for many years to exert anti-inflammatory effects in liver diseases ( Yang et al, 2021 ). Baicalin is also a Chinese botanical drug used to treat NASH.…”

Section: Pharmacological Agents Associated With Nlrp3 Inflammasome Su...mentioning

confidence: 99%

The NLRP3 Inflammasome in Non-Alcoholic Fatty Liver Disease and Steatohepatitis: Therapeutic Targets and Treatment

Wang

et al. 2022

Front. Pharmacol.

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Non-alcoholic fatty liver disease (NAFLD) is among the most prevalent primary liver diseases worldwide and can develop into various conditions, ranging from simple steatosis, through non-alcoholic steatohepatitis (NASH), to fibrosis, and eventually cirrhosis and hepatocellular carcinoma. Nevertheless, there is no effective treatment for NAFLD due to the complicated etiology. Recently, activation of the NLPR3 inflammasome has been demonstrated to be a contributing factor in the development of NAFLD, particularly as a modulator of progression from initial hepatic steatosis to NASH. NLRP3 inflammasome, as a caspase-1 activation platform, is critical for processing key pro-inflammatory cytokines and pyroptosis. Various stimuli involved in NAFLD can activate the NLRP3 inflammasome, depending on the diverse cellular stresses that they cause. NLRP3 inflammasome-related inhibitors and agents for NAFLD treatment have been tested and demonstrated positive effects in experimental models. Meanwhile, some drugs have been applied in clinical studies, supporting this therapeutic approach. In this review, we discuss the activation, biological functions, and treatment targeting the NLRP3 inflammasome in the context of NAFLD progression. Specifically, we focus on the different types of therapeutic agents that can inhibit the NLRP3 inflammasome and summarize their pharmacological effectiveness for NAFLD treatment.

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Section: Pharmacological Agents Associated With Nlrp3 Inflammasome Su...mentioning

confidence: 99%

The NLRP3 Inflammasome in Non-Alcoholic Fatty Liver Disease and Steatohepatitis: Therapeutic Targets and Treatment

Wang

et al. 2022

Front. Pharmacol.

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“…Baicalin (C 21 H 18 O 11 ) is an active flavonoid originat-ing from the root of Scutellaria baicalensis Georgi, which exerts anti-inflammatory and antioxidant effects in liver diseases [11]. Baicalin has various pharmacological activities, including antitumor, antimicrobial and antioxidant effects, with wide clinical applications [12][13][14]. However, whether baicalin has protective effects on hepatocyte lipotoxicity and the associated mechanism remain elusive.…”

Section: Introductionmentioning

confidence: 99%

Baicalin Attenuates Oxidative Stress in a Tissue-Engineered Liver Model of NAFLD by Scavenging Reactive Oxygen Species

Gao

Zhang

et al. 2022

Nutrients

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Oxidative stress plays an important role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Baicalin has been shown to exert protective effects in various liver diseases. The mechanism of baicalin’s antioxidative effect in NAFLD is currently unclear. The aim of this study was to investigate the effects and mechanisms of baicalin on oxidative stress in a new tissue-engineered liver model of NAFLD. The 3D model of NAFLD was induced by a fat-supplemented medium (fatty acids, FFA group) for 8 days and baicalin was administered on the 5th day. CCK-8 assay showed that baicalin at concentrations below 100 μM had no obvious cytotoxicity. Baicalin inhibited apoptosis and lactate dehydrogenase release in the FFA group. Baicalin reduced the levels of reactive oxygen species and malondialdehyde induced by FFA, and increased superoxide dismutase and glutathione amounts. However, it did not upregulate nuclear erythroid 2-related factor 2 compared with the FFA group. Mitochondrial morphology was partially restored after baicalin treatment, and ATP5A expression and mitochondrial membrane potential were increased. The superoxide anion scavenging ability of baicalin was enhanced in a dose-dependent manner. In summary, baicalin reduces oxidative stress and protects the mitochondria to inhibit apoptosis in the 3D NAFLD model via its own antioxidant activity.

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“…Baicalin regulates intestinal immunity and protects against intestinal damage due to ulcerative colitis and sepsis [ 12 , 13 ]. Baicalin protects against several types of liver diseases including viral hepatitis, fatty liver disease, xenobiotic-induced liver injury, cholestatic liver injury, and hepatocellular carcinoma, with a variety of pharmacological mechanisms [ 14 ]. It reverses the epithelial–mesenchymal transition through the inhibition of the TGF-β1/Smad3 pathway in vitro to prevent the development of liver fibrosis [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Baicalin Alleviates Short-Term Lincomycin-Induced Intestinal and Liver Injury and Inflammation in Infant Mice

Zhang

Zhong

Tang

et al. 2022

IJMS

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The adverse effects of short-term megadose of antibiotics exposure on the gastrointestinal and liver tissue reactions in young children have been reported. Antibiotic-induced intestinal and liver reactions are usually unpredictable and present a poorly understood pathogenesis. It is, therefore, necessary to develop strategies for reducing the adverse effects of antibiotics. Studies on the harm and rescue measures of antibiotics from the perspective of the gut–liver system are lacking. Here, we demonstrate that lincomycin exposure reduced body weight, disrupted the composition of gut microbiota and intestinal morphology, triggered immune-mediated injury and inflammation, caused liver dysfunction, and affected lipid metabolism. However, baicalin administration attenuated the lincomycin-induced changes. Transcriptome analysis showed that baicalin improved immunity in mice, as evidenced by the decreased levels of intestinal inflammatory cytokines and expression of genes that regulate Th1, Th2, and Th17 cell differentiation, and inhibited mucin type O-glycan biosynthesis pathways. In addition, baicalin improved liver function by upregulating the expression of genes involved in bile acid secretion and lipid degradation, and downregulating genes involved in lipid synthesis in lincomycin-treated mice. Bile acids can regulate intestinal immunity and strengthen hepatoenteric circulation. In addition, baicalin also improved anti-inflammatory bacteria abundance (Blautia and Coprobacillus) and reduced pathogenic bacteria abundance (Proteobacteria, Klebsiella, and Citrobacter) in lincomycin-treated mice. Thus, baicalin can ameliorate antibiotic-induced injury and its associated complications such as liver disease.

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Pharmacological properties of baicalin on liver diseases: a narrative review

Cited by 61 publications

References 101 publications

The NLRP3 Inflammasome in Non-Alcoholic Fatty Liver Disease and Steatohepatitis: Therapeutic Targets and Treatment

The NLRP3 Inflammasome in Non-Alcoholic Fatty Liver Disease and Steatohepatitis: Therapeutic Targets and Treatment

Baicalin Attenuates Oxidative Stress in a Tissue-Engineered Liver Model of NAFLD by Scavenging Reactive Oxygen Species

Baicalin Alleviates Short-Term Lincomycin-Induced Intestinal and Liver Injury and Inflammation in Infant Mice

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