Caffeic acid abrogates 1,3-dichloro-2-propanol-induced hepatotoxicity by upregulating nuclear erythroid-related factor 2 and downregulating nuclear factor-kappa B

Human and Experimental Toxicology - Tập 38 Số 9 - Trang 1092-1101 - 2019
TO Ajiboye1, RA Ajala-Lawal1, AB Adeyiga1
1Antioxidants, Redox Biology and Toxicology Research Laboratory, Department of Medical Biochemistry, College of Health Sciences, Nile University of Nigeria, FCT-Abuja, Nigeria

Tóm tắt

1,3-dichloro-2-propanol is a food-borne contaminant reported to cause liver injury. In this study, we evaluated the protective influence of caffeic acid on 1,3-dichloro-2-propanol-induced hepatotoxicity in rats. Rats were randomized into five groups (A–E). Rats received distilled water or caffeic acid (10 or 20 mg/kg body weight) for 7 days. In addition, rats were challenged with 1,3-dichloro-2-propanol on day 7. Caffeic acid prevented 1,3-dichloro-2-propanol-mediated alterations in alkaline phosphatase, alanine and aspartate aminotransferases, albumin and total bilirubin in the serum of rats. Furthermore, caffeic acid lowered superoxide ion, hydrogen peroxide and cytochrome P2E1 while increasing the activities of superoxide dismutase, catalase and glutathione S-transferase in the liver of 1,3-dichloro-2-propanol-treated rats. Caffeic acid raised the levels of nuclear erythroid-related factor 2 (Nrf-2), protein kinase A and phosphoinositide 3-kinase. Caffeic acid pretreatment annulled 1,3-dichloro-2-propanol-mediated alterations in the oxidative stress biomarkers; caspase-3, glutathione, malondialdehyde, protein carbonyl and fragmented DNA, in the liver of rats. Contrastingly, caffeic acid lowered 1,3-dichloro-2-propanol-mediated increase in the levels of nuclear factor-kappa B (NF-κB), tumour necrosis factor-α, interleukin-1β (IL-1β) and IL-6. In addition, caffeic acid preserved the morphological features of 1,3-dichloro-2-propanol-treated rats. Results from this study revealed that caffeic acid protects against 1,3-dichloro-2-propanol-induced hepatotoxicity by enhancing the cytoprotective enzymes through Nrf-2 while lowering inflammation through NF-κB.

Từ khóa


Tài liệu tham khảo

10.1007/s13273-016-0023-0

10.1016/j.etap.2017.07.013

10.1016/j.fct.2013.05.024

10.5625/lar.2016.32.1.24

10.1016/j.jfca.2008.04.010

10.1016/j.etap.2015.06.011

10.1016/j.yrtph.2008.11.001

10.1016/j.reprotox.2009.07.003

10.1080/13813455.2017.1415938

10.1016/S0300-483X(02)00196-8

10.1016/j.fbio.2013.03.003

10.1016/S0300-483X(02)00198-1

10.1371/journal.pone.0148042

10.1016/j.biopha.2018.02.051

10.1002/jbt.21517

10.1002/0471140864.ps0304s48

Wright PJ, 1972, Enzymologia, 42, 317

10.1016/j.micpath.2015.11.020

10.1016/S0021-9258(19)45228-9

10.1002/0471140856.tx0707s27

10.1016/S0021-9258(19)42083-8

10.1016/0304-4165(90)90086-C

10.1042/bj0620315

10.1016/0003-9861(59)90090-6

10.1038/nprot.2006.378

Reilly CA, 2001, Curr Protoc Toxicol

Levine RL, 1990, Oxygen radicals in biological systems Part B: Oxygen radicals and antioxidants, Vol. 186

10.1016/j.jep.2015.01.026

10.1111/jfbc.12479

10.1089/jmf.2013.0157

10.1080/01480545.2018.1523187

10.1016/j.cbi.2010.03.022

10.1016/j.fct.2012.12.042

10.1080/13880209.2017.1317819

10.3109/01480540903170746

10.3109/01480545.2010.536767

10.1177/0960327109357218

10.3748/wjg.v21.i13.3893

10.1002/jbt.22055

10.1016/j.freeradbiomed.2015.12.024

10.1016/j.canlet.2004.09.042

10.1055/s-0028-1088302

10.1002/jbt.21598

10.1002/jbt.21814

10.1016/j.freeradbiomed.2009.05.032

Thông tin
Thông tin xuất bản

Human and Experimental Toxicology

Tập 38 Số 9

1092-1101

Thông tin tác giả