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Connexin43 and Angiotensin II Alterations in Hearts of Rats Having Undergone an Acute Exposure to Alcohol

Huang, Quan-Yong MD*; Li, Xue-Fang*; Liu, Shui-Ping MD

The American Journal of Forensic Medicine and Pathology: March 2013 - Volume 34 - Issue 1 - p 68–71
doi: 10.1097/PAF.0b013e31827bf67f
Original Articles

Introduction Alcohol-induced heart damage is associated with enzyme and protein alterations. The purpose of this study was to investigate alcohol-induced alterations in cardiac connexin 43 (Cx43) and angiotensin II (Ang II) after acute alcohol administration.

Method Male Wistar rats were randomly divided into 2 groups: a control group and an ethanol group. The ethanol group intraperitoneally received 3.8 g/kg ethanol; the controls were given the same amount of saline via the same route. After the righting reflex disappeared, midsternotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of Cx43 and Ang II. Sections were analyzed by digital image analysis.

Result The expression of Cx43 was significantly reduced after acute ethanol treatment, with the integrated optical density lower when compared with control (P < 0.05). The expression of Ang II was significantly increased after acute ethanol treatment, supported by integrated optical density when compared with control (P < 0.05).

Conclusions In summary, cardiac protein expression of Cx43 and Ang II were found to be significantly altered after acute ethanol treatment, suggesting that these 2 proteins may be important underlying mechanisms of vulnerability to oxidative injury in the heart during acute ethanol. The present study indicated that acute ethanol toxicity caused different alterations in heart proteins that would be related to oxidative stress.

From the *Department of Pathology, School of Basic Medical Sciences, Dali University, Dali, Yunnan Province; and †Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.

Manuscript received June 30, 2011; accepted January 16, 2012.

The authors report no conflict of interest.

This study was supported by a grant from the Natural Science Foundation of Guangdong Province, China (4203003) and Guangdong Medical College (No:XQ0426).

Reprints: Quan-Yong Huang, MD, Department of Pathology, School of Basic Medical Sciences, Dali University, Xiaguan Wanhua Rd, Dali, Yunnan province 671000, China. E-mail:

© 2013 Lippincott Williams & Wilkins, Inc.