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127 results on '"Chen, Da-zhi"'

3. Corrigendum to ’ Cannabinoid receptors are involved in the protective effect of a novel curcumin derivative C66 against CCl4-induced liver fibrosis’ European Journal of Pharmacology 779 (2016) 20–30/ doi: 10.1016/j.ejphar.2016.02.067

Author

Huang, Si-Si, primary, Chen, Da-zhi, additional, Wu, He, additional, Chen, Rui-Cong, additional, Du, Shan-Jie, additional, Dong, Jia-Jia, additional, Liang, Guang, additional, Xu, Lan-Man, additional, Wang, Xiao-Dong, additional, Yang, Yong-Ping, additional, Yu, Zhen-Ping, additional, Feng, Wen-Ke, additional, and Chen, Yong-Ping, additional

Published
2024
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10. Attenuation of Experimental Autoimmune Hepatitis in Mice with Bone Mesenchymal Stem Cell-Derived Exosomes Carrying MicroRNA-223-3p

Author

Lu, Feng-Bin, Chen, Da-Zhi, Chen, Lu, Hu, En-De, Wu, Jin-Lu, Li, Hui, Gong, Yue-Wen, Lin, Zhuo, Wang, Xiao-Dong, Li, Ji, Jin, Xiao-Ya, Xu, Lan-Man, and Chen, Yong-Ping

Subjects
Male, STAT3 Transcription Factor, Macrophages, autoimmune liver disease, Mesenchymal Stem Cells, Articles, exosomes, Immunomodulation, Mice, Inbred C57BL, Disease Models, Animal, Hepatitis, Autoimmune, Mice, MicroRNAs, RAW 264.7 Cells, Liver, Animals, Cytokines, mesenchymal stromal cells, immunomodulatory, Cells, Cultured
Abstract

MicroRNA-223-3p (miR-223-3p) is one of the potential microRNAs that have been shown to alleviate inflammatory responses in pre-clinical investigations and is highly encased in exosomes derived from bone mesenchymal stem cells (MSC-exosomes). MSC-exosomes are able to function as carriers to deliver microRNAs into cells. Autoimmune hepatitis is one of the challenging liver diseases with no effective treatment other than steroid hormones. Here, we examined whether MSC-exosomes can transfer miR-223-3p to treat autoimmune hepatitis in an experimental model. We found that MSC-exosomes were successfully incorporated with miR-223-3p and delivered miR-223-3p into macrophages. Moreover, there was no toxic effect of exosomes on the macrophages. Furthermore, treatments of either exosomes or exosomes with miR-223-3p successfully attenuated inflammatory responses in the liver of autoimmune hepatitis and inflammatory cytokine release in both the liver and macrophages. The mechanism may be related to the regulation of miR-223-3p level and STAT3 expression in the liver and macrophages. These results suggest that MSC-exosomes can be used to deliver miR-223-3p for the treatment of autoimmune hepatitis.

Published
2019

15. MicroRNA-29c Acting on FOS Plays a Significant Role in Nonalcoholic Steatohepatitis Through the Interleukin-17 Signaling Pathway

Author

Cai, Chao, primary, Chen, Da-Zhi, additional, Tu, Han-Xiao, additional, Chen, Wen-Kai, additional, Ge, Li-Chao, additional, Fu, Tian-Tian, additional, Tao, Ying, additional, Ye, Sha-Sha, additional, Li, Ji, additional, Lin, Zhuo, additional, Wang, Xiao-Dong, additional, Xu, Lan-Man, additional, and Chen, Yong-Ping, additional

Published
2021
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18. Indole-3-carbinol and diindolylmethane induce apoptosis of human cervical cancer cells and in murine HPV16-transgenic preneoplastic cervical epithelium. (Nutrition and Cancer)

Author

Chen, Da-Zhi, Qi, Mei, Auborn, Karen J., and Carter, Timothy H.

Subjects
Cervical cancer -- Physiological aspects, Indole -- Health aspects, Cell death -- Physiological aspects, Antioxidants -- Health aspects, Food/cooking/nutrition
Abstract

Dietary indole-3-carbinol (I3C) has clinical benefits for both cervical cancer and laryngeal papillomatosis, and causes apoptosis of breast cancer cells in vitro. We asked whether I3C and its major acid-catalyzed condensation product diindolylmethane (DIM), which is produced in the stomach after consumption of cruciferous vegetables, could induce apoptosis of cervical cancer cell lines. We also asked whether this effect could be observed in vivo. In vitro, both I3C and DIM caused accumulation of DNA strand breaks in three cervical cancer cell lines. Induction of apoptosis was confirmed by nuclear morphology, nucleosome leakage, altered cytoplasmic membrane permeability and caspase 3 activation. Neither I3C nor DIM caused apoptotic changes in normal human keratinocytes. In C33A cervical cancer cells, DIM was more potent than I3C [dose at which the number of viable cells was 50% of that in untreated cultures ([LD.sub.50]) = 50-60 [micro]mol/L for DIM and 200 [micro]mol/L for I3C in a mitochondrial function assay] and faster acting. Furthermore, I3C reduced Bcl-2 protein in a time- and dose-dependent manner. In HPV16-transgenic mice, which develop cervical cancer after chronic estradiol exposure, apoptotic cells were detected in cervical epithelium by TdT-mediated dUTP nick-end labeling staining and by immunohistochemical staining of active caspase 3 only in mice exposed to 17 [beta]-estradiol ([E.sub.2]) and fed I3C. Rare apoptotic cells were also observed by hematoxylin and eosin staining in the spinous layer of the cervical epithelium in both control and transgenic mice. Estradiol reduced the percentage of these late-stage apoptotic cells in the cervical epithelium of transgenic, [E.sub.2]-treated mice, but this reduction was prevented by I3C. These data confirm the proapoptotic action of I3C on transformed cells in vitro, extend the observations to cervical cancer cells and to DIM and show for the first time that dietary I3C results in increased apoptosis in target tissues in vivo. KEY WORDS: * cervical cancer * indole-3-carbinol * diindolylmethane * apoptosis * mice

Published
2001

21. High fiber dietary and sodium butyrate attenuate experimental autoimmune hepatitis through regulation of immune regulatory cells and intestinal barrier

Author

Hu, En-De, primary, Chen, Da-Zhi, additional, Wu, Jin-Lu, additional, Lu, Feng-Bin, additional, Chen, Lu, additional, Zheng, Ming-Hua, additional, Li, Hui, additional, Huang, Yu, additional, Li, Ji, additional, Jin, Xiao-Ya, additional, Gong, Yue-Wen, additional, Lin, Zhuo, additional, Wang, Xiao-Dong, additional, Xu, Lan-Man, additional, and Chen, Yong-Ping, additional

Published
2018
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25. Sodium butyrate ameliorates S100/FCA-induced autoimmune hepatitis through regulation of intestinal tight junction and toll-like receptor 4 signaling pathway

Author

Wu, Jin-Lu, primary, Zou, Jia-Yun, additional, Hu, En-De, additional, Chen, Da-Zhi, additional, Chen, Lu, additional, Lu, Feng-Bin, additional, Xu, Lan-Man, additional, Zheng, Ming-Hua, additional, Li, Hui, additional, Huang, Yu, additional, Jin, Xiao-Ya, additional, Gong, Yue-Wen, additional, Lin, Zhuo, additional, Wang, Xiao-Dong, additional, Zhao, Ming-Fang, additional, and Chen, Yong-Ping, additional

Published
2017
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34. Plumbagin Ameliorates CCl 4 -Induced Hepatic Fibrosis in Rats via the Epidermal Growth Factor Receptor Signaling Pathway.

Author

Chen, Si, Chen, Yi, Chen, Bi, Cai, Yi-jing, Zou, Zhuo-lin, Wang, Jin-guo, Lin, Zhuo, Wang, Xiao-dong, Fu, Li-yun, Hu, Yao-ren, Chen, Yong-ping, and Chen, Da-zhi

Abstract

Epidermal growth factor (EGF) and its signaling molecules, EGFreceptor (EGFR) and signal transducer and activator of transcription factor 3 (STAT3), have been considered to play a role in liver fibrosis and cirrhosis. Plumbagin (PL) is an extracted component from the plant and has been used to treat different kinds of cancer. However, its role in regulation of EGFR and STAT3 during liver fibrosis has not been investigated. In this study, the effects of PL on the regulation of EGFR and STAT3 were investigated in carbon tetrachloride (CCl4) induced liver fibrosis and hepatic stellate cells (HSC-T6). PL significantly attenuated liver injury and fibrosis in CCl4 treated rats. At concentrations of 2 to 6 μM, PL did not induce significant cytotoxicity of HSC-T6 cells. Moreover, PL reduced phosphorylation of EGFR and STAT3 in both fibrotic liver and heparin-binding EGF-like growth factor (HB-EGF) treated HSC-T6 cells. Furthermore, PL reduced the expression of α-SMA, EGFR, and STAT3 in both fibrotic liver and HB-EGF treated HSC-T6 cells. In conclusion, plumbagin could ameliorate the development of hepatic fibrosis through its downregulation of EGFR and STAT3 in the liver, especially in hepatic stellate cells. [ABSTRACT FROM AUTHOR]

Published
2015
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35. Pathogenic role of HMGB1 in SARS?

Author

Chen, Guoqian, primary, Chen, Da-zhi, additional, Li, Jianhua, additional, Czura, Christopher J., additional, Tracey, Kevin J., additional, Sama, Andrew E., additional, and Wang, Haichao, additional

Published
2004
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