Atorvastatin, Losartan and Captopril Lead to Upregulation of TGF-[beta], and Downregulation of IL-6 in Coronary Artery Disease and Hypertension

Coronary artery disease (CAD) and hypertension are the main reasons of ischemic heart diseases (IHDs). Cytokines as the small glycoproteins are the main arm of immune system and manipulate all of the cardiovascular diseases. The aim of the current study was to examine the effects of treatment of hyp...

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Veröffentlicht in:PloS one 2016-12, Vol.11 (12), p.e0168312
Hauptverfasser: Sepehri, Zahra, Masoumi, Mohammad, Ebrahimi, Nazanin, Kiani, Zohre, Nasiri, Ali Akbar, Kohan, Farhad, Sheikh Fathollahi, Mahmood, Kazemi Arababadi, Mohammad, Asadikaram, Gholamreza
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Sprache:eng
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Zusammenfassung:Coronary artery disease (CAD) and hypertension are the main reasons of ischemic heart diseases (IHDs). Cytokines as the small glycoproteins are the main arm of immune system and manipulate all of the cardiovascular diseases. The aim of the current study was to examine the effects of treatment of hypertension and CAD on serum levels of IL-6, IL-8, TGF-[beta] and TNF-[alpha]. This interventional study was performed on the patients with hypertension without CAD (group 1), hypertension and CAD (group 2), CAD but not hypertension (group 3) and without hypertension and CAD as controls (group 4). The patients received routine treatment for hypertension and CAD. Serum levels of IL-6, IL-8, TGF-[beta] and TNF-[alpha] were analyzed in the groups treated with various drugs, using ELISA technique. With regard to the medications, Atorvastatin, Losartan and Captopril were administered more in patients (groups 1, 2 and 3) than the patients without hypertension and CAD. The results revealed that serum levels of TGF-[beta] and IL-6 were significantly increased and decreased, respectively, in the groups 1, 2 and 3 when compared to group 4. Serum levels of TGF-[beta] were also increased in females in comparison to males in the group 4. According to the results it seems that Atorvastatin, Losartan and Captopril have reduced inflammation in in vivo conditions via downregulation of IL-6 and upregulation of TGF-[beta].
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0168312