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Caffeic acid phenethyl ester inhibits liver fibrosis in rats.
World J Gastroenterol. 2015 Apr 07; 21(13):3893-903.WJ

Abstract

AIM

To investigate the hepatoprotective effects and antioxidant activity of caffeic acid phenethyl ester (CAPE) in rats with liver fibrosis.

METHODS

A total of 75 male Sprague-Dawley rats were randomly assigned to seven experimental groups: a normal group (n = 10), a vehicle group (n = 10), a model group (n = 15), a vitamin E group (n = 10), and three CAPE groups (CAPE 3, 6 and 12 mg/kg, n = 10, respectively). Liver fibrosis was induced in rats by injecting CCl4 subcutaneously, feeding with high fat forage, and administering 30% alcohol orally for 10 wk. Concurrently, CAPE (3, 6 and 12 mg/kg) was intraperitoneally administered daily for 10 wk. After that, serum total bilirubin (TBil), aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured to assess hepatotoxicity. To investigate antioxidant activity of CAPE, malondialdehyde (MDA), glutathione (GSH) levels, catalase (CAT) and superoxide dismutase (SOD) activities in liver tissue were determined. Moreover, the effect of CAPE on α-smooth muscle actin (α-SMA), a characteristic hallmark of activated hepatic stellate cells (HSCs), and NF-E2-related factor 2 (Nrf2), a key transcription factor for antioxidant systems, was investigated by immunohistochemistry.

RESULTS

Compared to the model group, intraperitoneal administration of CAPE decreased TBil, ALT, and AST levels in liver fibrosis rats (P < 0.05), while serum TBil was decreased by CAPE in a dose-dependent manner. In addition, the liver hydroxyproline contents in both the 6 and 12 mg/kg CAPE groups were markedly lower than that in the model group (P < 0.05 and P < 0.001, respectively). CAPE markedly decreased MDA levels and, in turn, increased GSH levels, as well as CAT and SOD activities in liver fibrosis rats compared to the model group (P < 0.05). Moreover, CAPE effectively inhibited α-SMA expression while increasing Nrf2 expression compared to the model group (P < 0.01).

CONCLUSION

The protective effects of CAPE against liver fibrosis may be due to its ability to suppress the activation of HSCs by inhibiting oxidative stress.

Authors+Show Affiliations

Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.Mei Li, Xiu-Fang Wang, Juan-Juan Shi, Ya-Ping Li, Ning Yang, Song Zhai, Shuang-Suo Dang, Department of Infectious Diseases, the Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710004, Shannxi Province, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25852274

Citation

Li, Mei, et al. "Caffeic Acid Phenethyl Ester Inhibits Liver Fibrosis in Rats." World Journal of Gastroenterology, vol. 21, no. 13, 2015, pp. 3893-903.
Li M, Wang XF, Shi JJ, et al. Caffeic acid phenethyl ester inhibits liver fibrosis in rats. World J Gastroenterol. 2015;21(13):3893-903.
Li, M., Wang, X. F., Shi, J. J., Li, Y. P., Yang, N., Zhai, S., & Dang, S. S. (2015). Caffeic acid phenethyl ester inhibits liver fibrosis in rats. World Journal of Gastroenterology, 21(13), 3893-903. https://doi.org/10.3748/wjg.v21.i13.3893
Li M, et al. Caffeic Acid Phenethyl Ester Inhibits Liver Fibrosis in Rats. World J Gastroenterol. 2015 Apr 7;21(13):3893-903. PubMed PMID: 25852274.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Caffeic acid phenethyl ester inhibits liver fibrosis in rats. AU - Li,Mei, AU - Wang,Xiu-Fang, AU - Shi,Juan-Juan, AU - Li,Ya-Ping, AU - Yang,Ning, AU - Zhai,Song, AU - Dang,Shuang-Suo, PY - 2014/08/24/received PY - 2014/10/25/revised PY - 2014/12/05/accepted PY - 2015/4/9/entrez PY - 2015/4/9/pubmed PY - 2016/1/21/medline KW - Caffeic acid phenethyl ester KW - Liver fibrosis KW - NF-E2-related factor 2 KW - Oxidative stress KW - α-smooth muscle actin SP - 3893 EP - 903 JF - World journal of gastroenterology JO - World J Gastroenterol VL - 21 IS - 13 N2 - AIM: To investigate the hepatoprotective effects and antioxidant activity of caffeic acid phenethyl ester (CAPE) in rats with liver fibrosis. METHODS: A total of 75 male Sprague-Dawley rats were randomly assigned to seven experimental groups: a normal group (n = 10), a vehicle group (n = 10), a model group (n = 15), a vitamin E group (n = 10), and three CAPE groups (CAPE 3, 6 and 12 mg/kg, n = 10, respectively). Liver fibrosis was induced in rats by injecting CCl4 subcutaneously, feeding with high fat forage, and administering 30% alcohol orally for 10 wk. Concurrently, CAPE (3, 6 and 12 mg/kg) was intraperitoneally administered daily for 10 wk. After that, serum total bilirubin (TBil), aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured to assess hepatotoxicity. To investigate antioxidant activity of CAPE, malondialdehyde (MDA), glutathione (GSH) levels, catalase (CAT) and superoxide dismutase (SOD) activities in liver tissue were determined. Moreover, the effect of CAPE on α-smooth muscle actin (α-SMA), a characteristic hallmark of activated hepatic stellate cells (HSCs), and NF-E2-related factor 2 (Nrf2), a key transcription factor for antioxidant systems, was investigated by immunohistochemistry. RESULTS: Compared to the model group, intraperitoneal administration of CAPE decreased TBil, ALT, and AST levels in liver fibrosis rats (P < 0.05), while serum TBil was decreased by CAPE in a dose-dependent manner. In addition, the liver hydroxyproline contents in both the 6 and 12 mg/kg CAPE groups were markedly lower than that in the model group (P < 0.05 and P < 0.001, respectively). CAPE markedly decreased MDA levels and, in turn, increased GSH levels, as well as CAT and SOD activities in liver fibrosis rats compared to the model group (P < 0.05). Moreover, CAPE effectively inhibited α-SMA expression while increasing Nrf2 expression compared to the model group (P < 0.01). CONCLUSION: The protective effects of CAPE against liver fibrosis may be due to its ability to suppress the activation of HSCs by inhibiting oxidative stress. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/25852274/Caffeic_acid_phenethyl_ester_inhibits_liver_fibrosis_in_rats_ L2 - https://www.wjgnet.com/1007-9327/full/v21/i13/3893.htm DB - PRIME DP - Unbound Medicine ER -