Publications by authors named "Jin-Rong Xia"

Now diabetes is growing to be a health problems globally. However, its specific pathogenesis still needs further exploration. Here we showed that miR-15b was upregulated in the palmitate-induced HepG2 cells and livers of hyperglycemic mice.

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Increasing evidence has suggested that hepatic lipid accumulation is associated with hepatic insulin resistance; however, the underlying mechanism is yet to be determined. It was demonstrated that the levels of microRNA‑215 (miR‑215) expression in the liver of rats fed a high‑fat diet were significantly increased compared with rats on a control diet. Additionally, it was revealed via luciferase assays and western blotting that miR‑215 targets rapamycin‑insensitive companion of mammalian target of rapamycin (Rictor), an important protein in the hepatic insulin signalling pathway.

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The aim of the present study was to investigate the effect of receptor for advanced glycation end products (RAGE)-specific small interfering (si)RNA on the generation of proinflammatory cytokines in primary rat hepatic stellate cells (HSCs) and hepatic fibrotic (HF) rats. The RAGE-specific siRNA expression vector pAKD-GR126 was constructed, and then transfected into primary rat HSCs. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were conducted to determine the mRNA and protein expression levels, respectively, of RAGE, tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the primary HSCs.

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Article Synopsis
  • The study's aim was to investigate how obesity and non-alcoholic fatty liver disease (NAFLD) impact the risk of developing type 2 diabetes mellitus (T2DM) among Chinese individuals.
  • A cohort of 4,847 subjects was sampled, with various health metrics collected at the start, followed by a four-year tracking of T2DM incidence to assess the relationship with body mass index (BMI) and NAFLD.
  • Results showed a significant higher incidence of T2DM in individuals with NAFLD (17.4%) compared to controls (4.1%), and obesity was also linked to increased T2DM risk, with obesity raising the hazard ratios for diabetes significantly after controlling for other health factors.
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Objective: This study was to specifically silence the minichromosome maintenance protein 7 (MCM7) expressions with lentivirus-mediated RNA interference technique in liver cancer MHCC-97H cells and its biological consequences were investigated.

Methods: Human MCM7 sequence was used for the design of shRNA targeting MCM7 which was then introduced to lentivirus, followed by transfection into MHCC-97H cells. Real time quantitative PCR and Western blot assay were performed to detect the mRNA and protein expression of MCM7 in these cells.

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Specific small interfering RNAs (siRNAs) targeting receptor for advanced glycation end products (RAGE) inhibit the expression of RAGE, α-smooth muscle actin and type I collagen in the T6 hepatic stellate cells (HSCs), indicating that RAGE is important for the activation of HSCs and the expression of collagen. The present study aimed to investigate the effect of specific siRNAs targeting RAGE on the development of hepatic fibrosis (HF), using primary rat HSCs, which were isolated and cultured in vitro. The expression vectors for specific siRNAs targeting RAGE were constructed and transfected into primary rat HSCs.

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Since the receptor for advanced glycation end products (RAGE)-ligand axis has been demonstrated to be important in fibrogenesis, rat models may be used to assess whether specific small interfering RNAs (siRNAs) that target RAGE are able to reduce the progression of hepatic fibrosis. However, the effect of RAGE-targeted siRNA on established hepatic fibrosis remains to be elucidated. In the present study, RAGE-specific siRNA expression vectors were constructed prior to the animal experiment.

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Cholangiocarcinoma (CCA) is a rare but devastating malignancy. Up to 90% of patients presenting with CCA have no identifiable risk factors. The base excision repair (BER) pathway has a principal role in the repair of mutations caused by oxidized or reduced bases.

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Receptor for advanced glycation end products (RAGE) was studied in different stages of carbon tetrachloride induced hepatic fibrosis (HF), and effect of its gene silencing in the HF development was evaluated in rats. Silencing RAGE expression by specific siRNA effectively suppressed NF-kappaB activity, hepatic stellate cell activation, and accumulation of extracellular matrix proteins in the fibrotic liver, and also greatly improved the histopathology and the ultrastructure of liver cells. These effects may be partially mediated by the inhibition on IkappaBalpha degradation.

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