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Intraductal Injection of LPS as a Mouse Model of Mastitis: Signaling Visualized via an NF-κB Reporter Transgenic
Published on: September 4, 2012
[Calcium-sensing receptor promotes endotoxin-induced myocardial injury through the JNK pathway]
Jia-Yu Song1, Jing Guo2, Chun-Ming Jiang1,3
1Department of Neonatology, the First Affiliated Hospital of Harbin Medical University, Harbin 150001.
Abstract:
Objective: To investigate the effects of calcium-sensing receptor (CaSR) on the c-Jun N-terminal kinase (JNK) in myocardial injury induced by endotoxin. Methods: The endotoxic model of neonatal rats was made by intraperitoneal injection of LPS(5 mg/kg). Neonatal Wistar rats were randomly divided into 6 groups: ①control group (saline group), ②endotoxin (LPS) group, ③LPS + CaSR agonist group, ④LPS + CaSR inhibitor group, ⑤LPS + JNK inhibitor group, ⑥LPS + CaSR inhibitor + JNK inhibitor group. The morphology of myocardium was observed by HE staining. The content of lactate dehydrogenase(LDH) in serum was determined. And the expression of IL-6 mRNA was detected by PCR. The protein expressions of CaSR and JNK were analyzed by Western blot. Results: Compared with the control group, the myocardial injury was aggravated in the LPS group. The content of LDH and the expressions of IL-6 mRNA, CaSR and JNK were increased significantly (P<0.05). Compared with the LPS group,myocardial injury was aggravated in the CaSR agonist group. The content of LDH and the expressions of IL-6 mRNA,CaSR and JNK were increased (P<0.05). In the CaSR inhibitor group,myocardial injury was reduced. The content of LDH and the expressions of CaSR and JNK were decreased (P<0.05). In the JNK inhibitor group,myocardial injury was further alleviated. The content of LDH and the expressions of IL-6 mRNA, CaSR and JNK were decreased (P<0.05). Myocardial injury was significantly reduced in the CaSR inhibitor + JNK inhibitor group. The content of LDH and the expressions of IL-6 mRNA, CaSR and JNK were further reduced (P<0.05). Conclusion: CaSR is involved in myocardial injury induced by LPS in neonatal rats perhaps through the JNK pathway.
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