Protective Effects of Yinchenhao Decoction on Cholesterol Gallstone in Mice Fed a Lithogenic Diet by Regulating LXR, CYP7A1, CYP7B1, and HMGCR Pathways

Meng, Yong; Meng, Ke; Zhao, Xin; Li, Donghua; Gao, Qingzhu; Wu, Shangwei; Y, Cui

doi:10.1155/2018/8134918

Cited by 7 publications

(3 citation statements)

References 48 publications

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“…Yinchenhao decoction [142], and ellagic acid [143]. These agents may be worth testing for their effectiveness in reducing early inflammatory responses in NAFLD.…”

Section: Targeting Mitochondrial Cholesterol Metabolites For Nash Int...mentioning

confidence: 99%

Mitochondrial Cholesterol Metabolites in a Bile Acid Synthetic Pathway Drive Nonalcoholic Fatty Liver Disease: A Revised “Two-Hit” Hypothesis

Kakiyama

Rodríguez‐Agudo

Pandak

2023

Cells

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The rising prevalence of nonalcoholic fatty liver disease (NAFLD)-related cirrhosis highlights the need for a better understanding of the molecular mechanisms responsible for driving the transition of hepatic steatosis (fatty liver; NAFL) to steatohepatitis (NASH) and fibrosis/cirrhosis. Obesity-related insulin resistance (IR) is a well-known hallmark of early NAFLD progression, yet the mechanism linking aberrant insulin signaling to hepatocyte inflammation has remained unclear. Recently, as a function of more distinctly defining the regulation of mechanistic pathways, hepatocyte toxicity as mediated by hepatic free cholesterol and its metabolites has emerged as fundamental to the subsequent necroinflammation/fibrosis characteristics of NASH. More specifically, aberrant hepatocyte insulin signaling, as found with IR, leads to dysregulation in bile acid biosynthetic pathways with the subsequent intracellular accumulation of mitochondrial CYP27A1-derived cholesterol metabolites, (25R)26-hydroxycholesterol and 3β-Hydroxy-5-cholesten-(25R)26-oic acid, which appear to be responsible for driving hepatocyte toxicity. These findings bring forth a “two-hit” interpretation as to how NAFL progresses to NAFLD: abnormal hepatocyte insulin signaling, as occurs with IR, develops as a “first hit” that sequentially drives the accumulation of toxic CYP27A1-driven cholesterol metabolites as the “second hit”. In the following review, we examine the mechanistic pathway by which mitochondria-derived cholesterol metabolites drive the development of NASH. Insights into mechanistic approaches for effective NASH intervention are provided.

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“…Yinchenhao decoction [142], and ellagic acid [143]. These agents may be worth testing for their effectiveness in reducing early inflammatory responses in NAFLD.…”

Section: Targeting Mitochondrial Cholesterol Metabolites For Nash Int...mentioning

confidence: 99%

Mitochondrial Cholesterol Metabolites in a Bile Acid Synthetic Pathway Drive Nonalcoholic Fatty Liver Disease: A Revised “Two-Hit” Hypothesis

Kakiyama

Rodríguez‐Agudo

Pandak

2023

Cells

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“…YCHD has been found to have a significant impact on various indicators, including sodium taurocholate cotransporting polypeptide, multidrug resistance protein 1, bile salt export pump, organic cation transporter 1, and organic anion transporter 1A2, leading to their increase. Furthermore, YCHD can regulate the main metabolic pathway of phase II, which inhibits the increase of naphthalene isothiocyanate content[ 98 ].…”

Section: The Treatment Of Oj: Medication and Surgerymentioning

confidence: 99%

Pathophysiological consequences and treatment strategy of obstructive jaundice

Liu¹,

Sun²,

Xu³

et al. 2023

World J Gastrointest Surg

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Obstructive jaundice (OJ) is a common problem in daily clinical practice. However, completely understanding the pathophysiological changes in OJ remains a challenge for planning current and future management. The effects of OJ are widespread, affecting the biliary tree, hepatic cells, liver function, and causing systemic complications. The lack of bile in the intestine, destruction of the intestinal mucosal barrier, and increased absorption of endotoxins can lead to endotoxemia, production of proinflammatory cytokines, and induce systemic inflammatory response syndrome, ultimately leading to multiple organ dysfunction syndrome. Proper management of OJ includes adequate water supply and electrolyte replacement, nutritional support, preventive antibiotics, pain relief, and itching relief. The surgical treatment of OJ depends on the cause, location, and severity of the obstruction. Biliary drainage, surgery, and endoscopic intervention are potential treatment options depending on the patient's condition. In addition to modern medical treatments, Traditional Chinese medicine may offer therapeutic benefits for OJ. A comprehensive search was conducted on PubMed for relevant articles published up to August 1970. This review discusses in detail the pathophysiological changes associated with OJ and presents effective strategies for managing the condition.

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“…Liver X receptor α (LXRα), an oxysterol-binding transcription factor, which regulate the transcription level of CYP7A1 . CYP7A1 was downregulated with lithogenic time progressed, while CYP7A1 mRNA was increased 3-fold under the treatment of Yinchenhao Decoction, and revealed that CYP7A1 mRNA may be efficient targets of Yinchenhao Decoction, which may be a preventive medicine against cholesterol gallstone formation (Meng et al 2018). CYP7A1 mediate the transformation of cholesterol into bile acids in vitro.…”

mentioning

confidence: 96%

Genetic Association of The CYP7A1 Gene with Duck Lipid Traits

Zhang

Qin

Luo

et al. 2018

Preprint

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Cholesterol 7α-hydroxylase (Cyp7a1) participates in lipid metabolism of liver, and its pathway involves catabolism of cholesterol to bile acids and excretion from the body. However, little is known about the effect of the polymorphisms of CYP7A1 gene on duck lipid traits. In the present study, seven novel synonymous mutations loci in exon 2 and exon 3 of CYP7A1 gene in Cherry Valley ducks were identified using PCR production direct sequencing. One novel SNP g.1033130 C>T was predicted in exon 2. Six novel SNPs g.1034076 C>T, g.1034334 G>A, g.1034373 G>A, g.1034448 T>C, g.1034541 C>G, and g.1034550 G>A were discovered in exon 3. Six haplotypes were detected using SHEsis online analysis software, and five loci (g.1034334G>A, g.1034373G>A, g.1034448T>C, g.1034541C>G, and g.1034550G>A) were in complete linkage disequilibrium, and as a block named Locus C3. By single SNP association analysis, we found that the g.1033130 C>T locus was significantly associated with IMF, AFP, TG, and TC (P<0.01 or P<0.05) respectively, the g.1034076 C>T locus was significantly associated with AFP (P<0.05), and the locus C3 was significantly associated with TCH (P<0.05). Sixteen dipoltypes were detected by the combination of haplotypes, and demonstrated strong association with IMF, AFP, TG, and TCH (P<0.01). Therefore, our data suggested that the seven SNPs of CYP7A1 gene are potential markers for lipid homeostasis, and may be used for early breeding and selection of duck.

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Protective Effects of Yinchenhao Decoction on Cholesterol Gallstone in Mice Fed a Lithogenic Diet by Regulating LXR, CYP7A1, CYP7B1, and HMGCR Pathways

Cited by 7 publications

References 48 publications

Mitochondrial Cholesterol Metabolites in a Bile Acid Synthetic Pathway Drive Nonalcoholic Fatty Liver Disease: A Revised “Two-Hit” Hypothesis

Mitochondrial Cholesterol Metabolites in a Bile Acid Synthetic Pathway Drive Nonalcoholic Fatty Liver Disease: A Revised “Two-Hit” Hypothesis

Pathophysiological consequences and treatment strategy of obstructive jaundice

Genetic Association of The CYP7A1 Gene with Duck Lipid Traits

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