Zhengzhou Childrens Hospital Zhengzhou 450053

Henan’an, China

Zhengzhou Childrens Hospital Zhengzhou 450053

Henan’an, China

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PubMed | Zhengzhou University and Zhengzhou Childrens Hospital Zhengzhou 450053
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2016

Ascorbic acid (AA) has been shown to exert beneficial effects, including mitigating oxidative stress and inhibiting inflammation. However, the preventative effect of vitamin C in chronic inammatory diseases such as inammatory bowel disease (IBD) remains unclear. In our study, we investigated the anti-inammatory effects of AA and possible mechanism involved in inhibiting dextran sulfate sodium (DSS)-induced ulcerative colitis in mice. Male C57BL/6 mice were randomly divided to three groups: control group, DSS group, and DSS plus ascorbic acid treated group. Several clinical and inammatory parameters as well as oxidative stress were evaluated. The results demonstrated that ascorbic acid signicantly reduced clinical signs, inammatory cytokines, myeloperoxidase (MPO) and malonaldehyde (MDA) activities, whereas the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were increased in DSS-induced mice. In addition, ascorbic acid was capable of inhibiting NF-B, COX-2 and iNOS expression in the colonic. Taken together, these findings suggest that ascorbic acid contributes to the reduction of oxidative stress and inammatory response in DSS-induced colitis and exerts the potential to prevent and clinical treatment of inammatory bowel disease.


PubMed | Zhengzhou University and Zhengzhou Childrens Hospital Zhengzhou 450053
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2015

Herpes simplex virus 1 (HSV-1) microRNAs (miRNAs) mostly located in transcription-associated transcript (LAT) region have been identified that play critical roles in the intricate host-pathogen interaction networks. Increasing evidences throw new insight into the role of miRNA-mediated miRNA-mRNA cross-talk in HSV-1 latent or acute infection. In the present study, we found that hsv-1 miR-H4-5p (here termed as miR-H4b) can down-regulate the expression of cyclin-dependent kinase inhibitor 2A (CDKN2A, p16) in neuroblastoma (SHSY5Y) cell lines. Decreased expression of miR-H4b was directly related to attenuated cell proliferation and invasion as well as malfunction of cell cycle in recombinant SHSY5Y cells that stably expressing miR-H4b. Bioinformatics analysis and luciferase assays demonstrated miR-H4b can directly target p16 mRNA. MiR-H4b exerts its pro-proliferation function through inhibition of the p16-related PI3K-Akt pathways. Our findings provide, for the first time, significant clues regarding the role of herpesvirus-encoded miRNAs as a viral modulator to host cells.

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