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Your search keyword '"Jin, Meilan"' showing total 9 results
Start Over Author "Jin, Meilan" Publisher sage publications
9 results on '"Jin, Meilan"'

1. Effect of berberine on LPS-induced expression of NF-κB/MAPK signalling pathway and related inflammatory cytokines in porcine intestinal epithelial cells

Author

Huang Jing, Xu Yuwei, Jin Meilan, Xiong Wen, Wang Zi-li, Li Xueying, Zhang Zhu, Li Chunlin, and Zeng Rongrong

Subjects
Lipopolysaccharides, lcsh:Immunologic diseases. Allergy, 0301 basic medicine, Berberine, Swine, Immunology, Anti-Inflammatory Agents, Pharmacology, Microbiology, NF-κB, Proinflammatory cytokine, 03 medical and health sciences, chemistry.chemical_compound, MAPKs, 0302 clinical medicine, Phellodendron, Escherichia coli, Animals, Phellodendron chinense, Intestinal Mucosa, Medicinal plants, Molecular Biology, Cells, Cultured, Escherichia coli Infections, Mitogen-Activated Protein Kinase Kinases, biology, Alkaloid, MAPK signalling, NF-kappa B, Original Articles, Cell Biology, Coptis chinensis, biology.organism_classification, 030104 developmental biology, Infectious Diseases, Gene Expression Regulation, chemistry, 030220 oncology & carcinogenesis, porcine intestinal epithelial cells inflammatory factors, Cytokines, Inflammation Mediators, lcsh:RC581-607, Coptis, Signal Transduction
Abstract

Berberine is an alkaloid extracted from medicinal plants such as Coptis chinensis and Phellodendron chinense. It possesses anti-inflammatory, anti-tumour and anti-oxidation properties, and regulates Glc and lipid metabolism. This study explored the mechanisms of the protective effects of berberine on barrier function and inflammatory damage in porcine intestinal epithelial cells (IPEC-J2) induced by LPS. We first evaluated the effects of berberine and LPS on cell viability. IPEC-J2 cells were treated with 5 μg/ml LPS for 1 h to establish an inflammatory model, and 75, 150 and 250 μg/ml berberine were used in further experiments. The expression of IL-1β, IL-6 and TNF-α was measured by RT-PCR. The key proteins of the NF-κB/MAPK signalling pathway (IκBα, p-IκBα, p65, p-p65, c-Jun N-terminal kinase (JNK), p-JNK, p38, p-p38, ERK1/2 and p-ERK1/2) were detected by Western blot. Upon exposure to LPS, IL-1β, IL-6 and TNF-α mRNA levels and p-IκBα p-p65 protein levels were significantly enhanced. Pre-treatment with berberine reduced the expression of inflammatory factors and was positively correlated with its concentration, and dose dependently inhibited the expression of IκBα, p-IκBα, p-p65, p-p38 and JNK. These results demonstrated that pre-treating intestinal epithelial cells with berberine was useful in preventing and treating diarrhoea induced by Escherichia coli in weaned pigs.

Published
2020

8. The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction.

Author

Xiong W, Ma H, Zhang Z, Jin M, Wang J, Xu Y, and Wang Z

Subjects
Apoptosis genetics, Caspase 3 genetics, Caspase 3 metabolism, Caspases, Initiator genetics, Caspases, Initiator metabolism, Catalase metabolism, Cell Survival drug effects, Endoplasmic Reticulum Chaperone BiP, Flavonoids metabolism, Glutathione Peroxidase metabolism, Goblet Cells enzymology, Goblet Cells metabolism, Heat-Shock Proteins genetics, Heat-Shock Proteins metabolism, Humans, Hydrogen Peroxide metabolism, Inflammation genetics, Interleukin-1beta metabolism, Interleukin-6 metabolism, Interleukin-8 metabolism, L-Lactate Dehydrogenase metabolism, Lipopolysaccharides pharmacology, Malondialdehyde metabolism, Mucin-2 biosynthesis, Mucin-2 metabolism, Phosphorylation, Reactive Oxygen Species metabolism, Superoxide Dismutase-1 metabolism, Transcription Factor CHOP genetics, Transcription Factor CHOP metabolism, Tumor Necrosis Factor-alpha metabolism, X-Box Binding Protein 1 genetics, X-Box Binding Protein 1 metabolism, Apoptosis drug effects, Cell Proliferation drug effects, Flavonoids pharmacology, Goblet Cells drug effects, Inflammation metabolism
Published
2020
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9. Molecular expression analysis of beta-naphthoflavone-induced hepatocellular tumors in rats.

Author

Dewa Y, Nishimura J, Jin M, Kawai M, Saegusa Y, Harada T, Shibutani M, and Mitsumori K

Subjects
Adenoma, Liver Cell genetics, Adenoma, Liver Cell metabolism, Animals, Body Weight, Cell Cycle Proteins genetics, Cell Cycle Proteins metabolism, Cell Proliferation, Data Interpretation, Statistical, Disease Models, Animal, Gene Expression Profiling, Histone Deacetylase 1, Histone Deacetylases metabolism, Immunohistochemistry, Liver metabolism, Liver pathology, Liver Neoplasms genetics, Liver Neoplasms metabolism, Oxidative Stress genetics, Proliferating Cell Nuclear Antigen metabolism, Rats, Receptors, Aryl Hydrocarbon agonists, Reverse Transcriptase Polymerase Chain Reaction, Adenoma, Liver Cell chemically induced, Enzyme Inhibitors toxicity, Liver Neoplasms chemically induced, beta-Naphthoflavone toxicity
Abstract

The present study was performed to characterize molecular expression levels of preneoplastic and neoplastic lesions induced by beta-naphthoflavone (BNF), an aryl hydrocarbon receptor (AhR) agonist in rat hepatocarcinogenesis. Male F344 rats were initiated with an intraperitoneal injection of 200 mg/kg N-diethylnitrosamine, and two weeks later, they were fed a diet containing 0% or 1% BNF for twenty-eight weeks. All animals were subjected to a two-thirds partial hepatectomy at week 3 and sacrificed at week 30. Histopathologically, BNF increased the incidence and multiplicity of altered foci (1.7-fold and 3.3-fold) and hepatocellular adenomas (HCAs) (4.0-fold and 4.7-fold). Immunohistochemically, BNF increased the number of proliferating cell nuclear antigen (PCNA)-positive cells in altered foci (2.3-fold) and HCAs (6.7-fold) compared with the surrounding tissue and decreased the staining of cell cycle regulators (P21, C/EBPalpha). In addition, loss of reactivity for AhR-regulated (CYP1A1, CYP1B1) molecules and increased reactivity of Nrf-2-regulated (AKR7, GPX2) molecules were also observed in proliferative lesions. Furthermore, increased staining of histone deacetylase (HDAC1) in the nucleus was prominent in HCAs. The differential expression patterns were confirmed at mRNA levels by real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis. These results suggest that enhanced cell proliferation and protection against oxidative stress play an important role in BNF-induced hepatocarcinogenesis in rats.

Published
2009
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