Publications by authors named "Maoxiang Yan"

Background And Aim: Nonalcoholic steatohepatitis (NASH) is a critical stage in the prognosis of nonalcoholic fatty liver disease (NAFLD). Pure total flavonoids from circus (PTFC) play essential roles in the improvement of NASH symptoms, but the underlying regulatory mechanism remains elusive. Our previous high-throughput omics screening results indicate that the CCL2/CCR2-PI3K-Akt signaling pathway is a key pathway that regulates the liver inflammatory response.

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With the continuous improvement of living standards but the lack of exercise, aging-associated metabolic diseases such as obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD) are becoming a lingering dark cloud over society. Studies have found that metabolic disorders are near related to glucose, lipid metabolism, and cellular aging. Fibroblast growth factor 21 (FGF21), a member of the FGFs family, efficiently regulates the homeostasis of metabolism and cellular aging.

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Background: Our previous studies found that Pure total flavnoids from citrus (PTFC) can effectively improve non-alcoholic steatohepatitis (NASH) in mice. Here, we discuss on the mechanism of PTFC in treating NASH with focus on the regulation of the gut microbiota and bile acid metabolism.

Methods: C57BL/6 J mice were randomly divided into three groups: normal diet group (Normal), high-fat diet group (HFD) and high-fat + PTFC treatment group (PTFC).

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To observe the therapeutic effect of berberine (BBR) on non-alcoholic steatohepatitis (NASH) in rats and the underlying mechanism. A rat model of NASH was established by a high-fat diet, and BBR was used as treatment. Haematoxylin-eosin staining and Oil Red O staining were used to observe the pathological changes in the liver tissue.

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Background: Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease worldwide. Recent studies have shown that the Angptl2 pathway mediated hepatic inflammatory response plays an important role in the progression of nonalcoholic fatty liver disease. Our study investigated the possible molecular mechanisms of berberine (BBR) in the treatment of the liver inflammatory response in the livers of rats with high-fat diet-induced NAFLD via the Angptl2 pathway.

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Objective: To investigate the effectiveness of Banxia Xiexin decoction (BXD) in a rat model of chronic atrophic gastritis (CAG).

Methods: Sixty 6-week-old healthy Wistar rats (30 males, 30 females) were used in the present study. A rat model of CAG was successfully established using the combined active immunization/ethanol/sodium deoxycholate method.

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Objective: To explore the changes of Sonic Hedgehog (Shh) signaling pathway in the stomach mucosa during the formation of gastric precancerous lesions.

Methods: A total of 72 suckling rats in half genders were randomly and equally divided into the normal group and model group. The rats in the model group were administered with 0.

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Objective: This study investigated the possible molecular mechanisms of pure total flavonoids from citrus (PTFC) for the treatment of non-alcoholic fatty liver disease (NAFLD) via toll-like receptor/C-C chemokine ligand (TLR/CCL) signaling pathways by monitoring the changes in gene expression profile in liver tissues induced by high-fat diet.

Methods: We performed systematical analyses on hepatic expression profiles of mRNAs in a high-fat diet (HFD)-induced steatotic animal model with or without PTFC treatment. The study was conducted by using MouseOneArray v2 gene chip, and analyzed by bioinformatics tools for differential gene expression.

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Background: Non-alcoholic fatty liver disease (NAFLD) is a common, chronic liver disease worldwide. Recent studies have shown that T helper (Th) 17 and regulatory T (Treg) cells play critical roles in various disorders of liver inflammation. Here, we explored the value of polyene phosphatidylcholine capsules (PPC) for regulating the imbalance of Th17/Treg cells in the pathogenesis of mice with NAFLD.

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Objective: To investigate the effect of total flavone of haw leaves (TFHL) on the expression of nuclear factor erythroid-2 related factor (Nrf2) and other related factors in nonalcoholic steatohepatitis (NASH) rats induced by high-fat diet and then to further discuss the mechanism of TFHL's prevention against NASH.

Methods: High-fat diet was fed to 40 rats to establish the NASH model. Then model rats were intragastrically administrated with 40, 80, 160 mg/(kg•day) TFHL, respectively.

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To explore the effect of total flavones from hawthorn leaf on (THFL) on the expression of COX-2/Nrf2 in the liver tissues of rats with nonalcoholic steatohepatitis (NASH), and discuss its anti-NASH mechanism, thirty-two SD rats were randomly divided into the normal group, model group, THFL high dose group and low dose group, 8 in each group. High fat diet was given to the rats for 12 weeks to establish the NASH models, and the high and low dose groups were administered with TFHL at the dosage of 250, 125 mg•kg⁻¹•d⁻¹ respectively. Steatosis and the inflammatory changes of the liver tissues in rats were observed by HE staining; T-AOC level was detected by colorimetry; the level of 8-OHdG and the protein expressions of COX-2, Nrf2 and HO-1 in the liver tissues were determined by immunohistochemistry; and the mRNA expressions of COX-2, Nrf2 and HO-1 in liver tissues were detected by Real time-PCR.

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To study the preventive effect of Grifola frondosa on nonalcoholic steatohepatitis (NASH). The rat model of NASH was established by feeding high-fat diets for 12 weeks and intervened with 0.5 g · kg(-1) · d(-1) and 1.

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Objective: To explore the role of NF-E2-related factor 2(Nrf2) and its related factors in the progression of nonalcoholi steatohepatitis (NASH) by investigating the alterations of lipid metabolism and liver histopathology as well as the changes of mRNA and protein expression levels of Nrf2 and its related factors in rats during NASH progression.

Methods: Male SD rats were randomly divided into normal group and model group, which were administrated with high fat diet to establish nonalcoholic steatohepatitis model. The rats from both groups were randomly killed at the end of 4, 12 weeks respectively.

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Objective: To observe the effect of pure total flavonoids from Citrus (PTFC) on the hepatic fatty degeneration, inflammation, oxidative stress and SIRT1/PGC-1alpha expressions in mice with non-alcohol steatohepatitis (NASH), and discuss the action mechanism of PTFC on NASH.

Method: Mice were given high-fat diet for 16 weeks to induce the NASH model. Since the seventh week after the model establishment, the mice were intervened with 100, 50 and 25 mg x kg(-1) x d(-1) PTFC for 10 weeks.

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Objective: To study the expression of uncoupling protein 2 (UCP2) in liver of rats with nonalcoholic steatohepatitis (NASH) induced by fat-rich diet, and the effect of total flavones of hawthorn leafon (TFHL) on UCP2.

Method: The NASH model of rat was induced by 12 weeks of fat-rich diet. Subsequently the rats were administrated with TFHL in accordance with 250, 125 mg x kg(-1) x d(-1) and the Essentiale N with 195.

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Objective: To observe the influences of FVP1 on both curative and negative effects of CTX.

Method: The present study included two parts of experiments. In the part 1, 0.

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