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Information Journal Paper

Title

Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-α , IL-6 inhibition, and SOCS1 activation

Pages

  1259-1266

Abstract

 Objective(s): Cirrhotic cardiomyopathy is a complication of uncured cirrhosis which is associated with hyporesponsiveness of the heart to sympathetic stimulation. The enhancement of portal pressure, nitric oxide (NO) level, pro-inflammatory mediators and down-regulation of Suppressor of Cytokine Signaling 1 (SOCS1) are involved in this situations. The present study seeks to examine the beneficial effect of Thalidomide on Cirrhotic cardiomyopathy. Materials and Methods: The male rats were grouped as: Sham/saline, Sham/Thalidomide, Bile Duct Ligation (BDL)/saline and BDL/Thalidomide. BDL model of cirrhosis was used. In the treatment groups, Thalidomide (200 mg/kg/day) was administrated by intragastrial gavage for 28 consecutive days, the chronotropic response was assessed in isolated atria by isoproterenol stimulation. Serum levels of NO, IL-6 and TNF-α hepatic level were evaluated. The intrasplenic pulp pressure (ISPP) as the portal pressure and histopathologic assessment were assessed. Real time RT-PCR was used for the evaluation of SOCS1 gene expression. Results: Our results showed that Thalidomide administration could significantly increase the atrial chronotropic response in BDL animals. The increased level of portal pressure decreased by Thalidomide in BDL animals. Thalidomide could ameliorate the histopathological conditions of BDL rats. Furthermore, the chronic treatment by this drug diminished the elevated levels of NO, TNF-α and IL-6 in BDL animals. On the other hand, hepatic SOCS1 expression was up-regulated by Thalidomide treatment in this group. Conclusion: Thalidomide improves the chronotropic hyporesponsiveness of isolated atria in BDL. This effect is probably mediated by the inhibiting NO, TNF-α and IL-6 production, reducing portal pressure and increasing the expression of SOCS1.

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    APA: Copy

    Hosseini Chegeni, Ali, JAZAERI, FARAHNAZ, Yousefi Ahmadipour, Aliakbar, HEIDARI, MANSOUR, Abdollahie, Alireza, & DEHPOUR, AHMAD REZA. (2019). Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-α , IL-6 inhibition, and SOCS1 activation. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, 22(11), 1259-1266. SID. https://sid.ir/paper/722825/en

    Vancouver: Copy

    Hosseini Chegeni Ali, JAZAERI FARAHNAZ, Yousefi Ahmadipour Aliakbar, HEIDARI MANSOUR, Abdollahie Alireza, DEHPOUR AHMAD REZA. Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-α , IL-6 inhibition, and SOCS1 activation. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES[Internet]. 2019;22(11):1259-1266. Available from: https://sid.ir/paper/722825/en

    IEEE: Copy

    Ali Hosseini Chegeni, FARAHNAZ JAZAERI, Aliakbar Yousefi Ahmadipour, MANSOUR HEIDARI, Alireza Abdollahie, and AHMAD REZA DEHPOUR, “Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-α , IL-6 inhibition, and SOCS1 activation,” IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, vol. 22, no. 11, pp. 1259–1266, 2019, [Online]. Available: https://sid.ir/paper/722825/en

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