Interleukin 10 Attenuates Angiotensin II-Induced Aortic Remodelling by Inhibiting Oxidative Stress-Induced Activation of the Vascular p38 and NF-κB Pathways

Abstract

Interleukin 10 (IL-10) is a probable anti-inflammatory factor that can attenuate hypertrophic remodelling caused by overloaded pressure and improve cardiac function. In this study, IL-10 was decreased in both the plasma of hypertensive patients and the aortic vessels of angiotensin II (Ang II)-induced hypertensive mice. IL-10 was unable to alter blood pressure in the case of Ang II-induced hypertension. The aortic thickness, collagen deposition, and the levels of fibrosis-associated markers, including collagen type I α 1 (Col1α1), connective tissue growth factor (CTGF), transforming growth factor-β (TGF-β), and matrix metalloproteinase 2 (MMP2), were significantly reduced in the IL-10 treatment group compared with the vehicle group after Ang II treatment. Moreover, IL-10 treatment significantly inhibited the number of CD45+ positive cells and the mRNA expression levels of proinflammatory cytokines in the vascular tissue of Ang II-infused mice. Furthermore, dihydroethidium (DHE) and 4hydroxynonenal (4-HNE) staining showed that IL-10 decreased Ang II-induced vascular oxidative stress and lipid peroxidation. Furthermore, IL-10 suppressed Ang II-induced proliferation, fibrosis, and inflammation of mouse vascular adventitial fibroblasts (mVAFs). Mechanistically, IL-10 suppressed the phosphorylation of p38 mitogen-activated protein (MAP) kinase and nuclear factor-κB (NF-κB) in Ang II-induced vascular fibrosis. In summary, our data indicated that IL-10, as a potential therapeutic target treatment, could limit the progression of Ang II-induced aortic remodelling.

Concurrent exercise training induces additional benefits to hydrochlorothiazide: Evidence for an improvement of autonomic control and oxidative stress in a model of hypertension and postmenopause

“…IL-10 treatment has been shown to improve SOD and CAT activities, as well as the redox ratio in renal ischemia-reperfusion induced by lipid peroxidation [ 56 ]. Recently, Qiu et al [ 57 ] demonstrated that IL-10 reverses AH-induced vascular hypertrophy, possibly through its antioxidant and anti-inflammatory effects. Moreover, Kaur et al [ 10 ] have highlighted the antioxidant properties of IL-10 by mitigating the antioxidant changes caused by TNF-α.…”

Modulation of TNF‐α, interleukin‐6, and interleukin‐10 by nebivolol–valsartan and nebivolol–lisinopril polytherapy in SHR rats

“…Aortic RNA extraction was performed using TRIzol reagent method 15 (Thermo Fisher Scientific, MA, USA). cDNA synthesis and polymerase chain reaction were performed using a QuantiNova SYBR® Green RT‐PCR Kit (QIAGEN, Gilden, Germany).…”

“…As such, IL-10 represents a potential therapeutic target for limiting the progression of Ang II-induced aortic remodeling. 15 Thus, acquiring a thorough comprehension of hypertension and its intricate connection with inflammation reveals promising new avenues for therapeutic interventions. Multiple studies have provided substantial evidence that monotherapy involving reninangiotensin system (RAS) inhibitors can modulate immune cell functions and regulate immune response mechanisms, not solely within the hypertensive patient population but across various other disease contexts as well.…”

“…Notably, IL‐10 levels were found to be decreased in the vessels of Ang II‐induced hypertensive mice. As such, IL‐10 represents a potential therapeutic target for limiting the progression of Ang II‐induced aortic remodeling 15 …”

“…As such, IL‐10 represents a potential therapeutic target for limiting the progression of Ang II‐induced aortic remodeling. 15 …”