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Bayat, Gholamreza, Mazloom, Roham, Hashemi, Seyed Ali, Pourkhalili, Khalil, Fallah, Parviz, Shams, Alireza, Esmaeili, Parvaneh, Khalili, Azadeh. (1401). Silymarin Administration Attenuates Cirrhotic-induced Cardiac Abnormality in the Rats: A Possible Role of β1-adrenergic Receptors and L-type Voltage-Dependent Calcium Channels. سامانه مدیریت نشریات علمی, 47(4), 367-378. doi: 10.30476/ijms.2021.90750.2172
Gholamreza Bayat; Roham Mazloom; Seyed Ali Hashemi; Khalil Pourkhalili; Parviz Fallah; Alireza Shams; Parvaneh Esmaeili; Azadeh Khalili. "Silymarin Administration Attenuates Cirrhotic-induced Cardiac Abnormality in the Rats: A Possible Role of β1-adrenergic Receptors and L-type Voltage-Dependent Calcium Channels". سامانه مدیریت نشریات علمی, 47, 4, 1401, 367-378. doi: 10.30476/ijms.2021.90750.2172
Bayat, Gholamreza, Mazloom, Roham, Hashemi, Seyed Ali, Pourkhalili, Khalil, Fallah, Parviz, Shams, Alireza, Esmaeili, Parvaneh, Khalili, Azadeh. (1401). 'Silymarin Administration Attenuates Cirrhotic-induced Cardiac Abnormality in the Rats: A Possible Role of β1-adrenergic Receptors and L-type Voltage-Dependent Calcium Channels', سامانه مدیریت نشریات علمی, 47(4), pp. 367-378. doi: 10.30476/ijms.2021.90750.2172
Bayat, Gholamreza, Mazloom, Roham, Hashemi, Seyed Ali, Pourkhalili, Khalil, Fallah, Parviz, Shams, Alireza, Esmaeili, Parvaneh, Khalili, Azadeh. Silymarin Administration Attenuates Cirrhotic-induced Cardiac Abnormality in the Rats: A Possible Role of β1-adrenergic Receptors and L-type Voltage-Dependent Calcium Channels. سامانه مدیریت نشریات علمی, 1401; 47(4): 367-378. doi: 10.30476/ijms.2021.90750.2172

Silymarin Administration Attenuates Cirrhotic-induced Cardiac Abnormality in the Rats: A Possible Role of β1-adrenergic Receptors and L-type Voltage-Dependent Calcium Channels

Iranian Journal of Medical Sciences
مقاله 10، دوره 47، شماره 4، مهر 2022، صفحه 367-378    اصل مقاله (1.66 M)
نوع مقاله: Original Article(s)
شناسه دیجیتال (DOI): 10.30476/ijms.2021.90750.2172
نویسندگان
Gholamreza Bayat1، 2؛ Roham Mazloom1؛ Seyed Ali Hashemi3؛ Khalil Pourkhalili4؛ Parviz Fallah5؛ Alireza Shams6؛ Parvaneh Esmaeili7؛ Azadeh Khalili* 1، 2
1Department of Physiology-Pharmacology-Medical Physics, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran
2Evidence-based Phytotherapy and Complementary Medicine Research Center, Alborz University of Medical Sciences, Karaj, Iran
3Department of Pathology, School of Medicine, Alborz University of Medical Sciences, Karaj Iran
4Department of Physiology, School of Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
5Department of Medical Laboratory Sciences, School of Para-Medicine, Alborz University of Medical Sciences, Karaj, Iran
6Department of Anatomy, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran
7EqlimDanesh Co. Ltd, Tehran, Iran
چکیده
Background: Cirrhotic cardiomyopathy is a well-recognized cardiac dysfunction in cirrhotic patients. Studies have confirmed the protective effects of silymarin in different types of cardiac injury. This study aimed to examine the effectiveness and molecular mechanism of silymarin against myocardial dysfunction and hypertrophy in a rat model of cirrhosis. 
Methods: The experiment was performed at Alborz University of Medical Sciences (Karaj, Iran) during 2020-2021. Thirty-two male Wistar rats were randomly divided into four groups of Sham-operated (control group for surgical procedures), Bile Duct Ligated (BDL), and two Silymarin extract (SE)-treated groups of 300 and 600 mg/Kg/day. After 28 days, serum levels of AST, ALT, GGT, and ALP, liver histopathological status, as well as cardiac mechanical function, were assessed. Cardiac β1-adrenergic receptors (β1-AR), L-type voltage-dependent calcium channels (L-VDCC), and GATA4 mRNA expression were also determined using real-time RT-PCR. Data analysis was performed using the one-way ANOVA followed by Duncan’s multiple range test. Histological data has been analyzed with Kruskal-Wallis nonparametric test. The analysis was performed at P≤0.05.
Results: BDL was associated with a significant elevation in serum AST, ALT, GGT, and ALP, development of necrosis and fibrosis of the liver texture, increased Heart Weight and Heart Weight to Body Weight ratio, enhanced cardiac mechanical function as well as a significant up-regulation of ventricular β1-AR and L-VDCC. Administration of SE600, but not SE300, significantly reduced the serum levels of the enzymes and alleviated signs of liver necrosis and fibrosis. Cirrhotic-induced cardiac dysfunction was also restored by SE600, but not by the lower dose. In addition, cardiac expression of the β1-AR and L-VDCC was down-regulated toward normal values by either higher or lower doses of the SE. 
Conclusion: Silymarin treatment in higher dose attenuated cirrhosis-associated cardiac remodeling and reduced cardiac mechanical dysfunctions.
کلیدواژه‌ها
Silymarin؛ Liver cirrhosis؛ Cardiomyopathies؛ Receptors, Adrenergic, beta؛ Calcium channels, L-type
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