E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Abstract

Abstract. Atropine-induced heart damage is associated with changes in the expression of various enzymes and proteins. The purpose of this study was to investigate atropine-induced alterations in cardiac E-cadherin and 5-hydroxytryptamine (5-HT) after atropine administration. Male Wistar rats were randomly divided into two groups: a control group and an atropine group. The atropine group intraperitoneally received atropine at a single dose of 15 mg/kg for 7 days; the controls received the same amount of saline via the same route. On Day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of E-cadherin and 5-HT. Sections were analyzed by digital image analysis. Cardiac protein expression of E-cadherin and 5-HT was altered after atropine-induced toxicity in the rat. The expression levels of E-cadherin and 5-HT were significantly decreased after atropine treatment, supported by IOD analysis, when compared with the control (P<0.05). The current findings indicate that such changes would be reflected in abnormal cardiac function, and these proteins may be useful for revealing the mechanisms underlying atropine-induced toxicity and may also provide various clues for further research.

Cytotoxicity of atropine to human corneal epithelial cells by inducing cell cycle arrest and mitochondrion-dependent apoptosis

“…These findings are also consistent with the report that downregulation of E-cadherin was involved in the toxicity of atropine to rat cardiac cells (Huang et al, 2012), and that of b-catenin involved in cell cycle arrest of mouse myoblasts and canine kidney-derived epithelial cells (Gavard et al, 2004;Orford, 1999). Taken together, our findings suggest that one of the cytotoxic mechanisms of atropine might be achieved by inducing cell cycle arrest of HCEP cells mediated by downregulation of E-cadherin and b-catenin.…”

The Effects of The Non-Fatal Electrical Injury on Caspase-3 Expression in Ovaries of Female Albino Rats: Histological and Immunohistochemical Study

“…We examined the negative control slide to exclude the target antigen specific labelling by primary antibody. The negative control sections were examined for the absence of specific staining to confirm the lack of cross-reactivity of secondary antibody and other non-target cell components (Huang et al, 2012).…”

Alterations in ACE and ABCG2 expression levels in the testes of rats subjected to atropine-induced toxicity

“…All procedures described in the present study were approved by the ethics committee of Dali University (Dali, China). Animals were randomly assigned to one of two groups (n=8 rats/group): The atropine group, which received intraperitoneal injections of a physiological dose of 15 mg/kg/day atropine for seven days (one injection per day) and the control group, which received identical volumes of normal saline for seven days (10).…”

“…Atropine has been shown to be cytotoxic to human corneal epithelial cells via the induction of cell cycle arrest and death receptor-mediated mitochondrion-dependent apoptosis (9). In the heart, atropine toxicity resulted in altered expression levels of E-cadherin and serotonin (10), and in the lung, atropine decreased pulmonary gas exchange in a dose-dependent manner (11). In addition, atropine alters pulse rate, pupil diameter and salivary flow (12).…”