Anti-Inflammatory Mechanism of Moderate Aerobic Exercise in Spleen: Focus on TLR4/PI3K/Akt Signaling Pathway

2017 ◽  
Vol 9 (4) ◽  
pp. 179-182
Author(s):  
Chien-Wei Chen
Keyword(s):  
Aerobic Exercise ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Inflammatory Mechanism ◽  
Anti Inflammatory

scholarly journals Thyroid hormone mediates cardioprotection against postinfarction remodeling and dysfunction through the IGF-1/PI3K/AKT signaling pathway

2020 ◽  
Author(s):  
Bin Zeng ◽  
Xiaoting Liao ◽  
Lei Liu ◽  
Caixia Zhang ◽  
Huaiyu Ruan
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Diseases ◽  
Thyroid Hormone ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Left Ventricular ◽  
Sham Operation ◽  
Akt Signaling Pathway ◽  
Anti Inflammatory ◽  
Related Proteins

Abstract Background Severe cardiovascular diseases, such as myocardial infarction or heart failure, can alter thyroid hormone (TH) secretion and peripheral conversion, leading to low triiodothyronine (T3) syndrome. Accumulating evidence suggests that TH has protective properties against cardiovascular diseases and that treatment with TH can effectively reduce myocardial damage after myocardial infarction (MI). However, the potential mechanisms are not clear. This study was designed to investigate the effect of T3 pretreatment on cardiac function and pathological changes in mice subjected to MI and the underlying mechanisms. Methods Adult male C57BL/6 mice underwent surgical ligation of the left anterior descending coronary artery (LAD) (or sham operation) to establish a myocardial infarction model. T3, BMS-754807 (inhibitor of insulin-like growth factor-1 receptor (IGF-1R)) or vehicle was administered before surgery. Results Compared with the MI group, the T3 pretreatment group exhibited significant attenuation of the myocardial infarct area, inhibition of cardiomyocyte apoptosis and fibrosis, and improved left ventricular function after MI. In addition, T3 exhibited an enhanced potency to stimulate angiogenesis and exert anti-inflammatory effects by reducing the levels of serum inflammatory cytokines after myocardial infarction. However, all of these protective effects were inhibited by the IGF-1R inhibitor BMS-754807. Moreover, the protein expression of IGF-1/PI3K/AKT signaling-related proteins, such as IGF-1, IGF-1R, phosphorylated PI3K (p-PI3K) and p-AKT was significantly upregulated in MI mice that received T3 pretreatment, and BMS-754807 pretreatment blocked the upregulation of the expression of these signaling-related proteins. Conclusion T3 pretreatment can protect the heart against dysfunction post-MI through its anti-apoptotic, anti-fibrotic, anti-inflammatory and angiogenesis-stimulating effects, which may be mediated by the activation of the IGF-1/PI3K/AKT signaling pathway.

scholarly journals AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway

2021 ◽  
Vol 11 (11) ◽  
pp. 1487
Author(s):  
Xiaojin Sun ◽  
Yang Deng ◽  
Xinxin Fu ◽  
Siyu Wang ◽  
Rui Duan ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Signaling Pathway ◽  
Renin Angiotensin System ◽  
Akt Signaling ◽  
Mouse Tissue ◽  
Morris Water Maze Test ◽  
Akt Signaling Pathway ◽  
Nissl Staining ◽  
Anti Inflammatory ◽  
The Brain

The renin-angiotensin system (RAS) is a paracrine RAS within the central nervous system (CNS) and is closely related to Alzheimer’s disease (AD). The endogenous hexapeptide angiotensin IV (Ang IV), an important component of the brain RAS, was found to rescue cognitive impairment and recover memory in previous studies. In our study, we used different doses of Dihexa, which can be orally administered and cross the BBB in APP/PS1 mice. We found that the amount of AngIV in mouse tissue increased after the administration of Dihexa compared to that in the WT group. Meanwhile, Dihexa restored spatial learning and cognitive functions in the Morris water maze test. Dihexa increased the neuronal cells and the expression of SYP protein in APP/PS1 mice in Nissl staining. Furthermore, Dihexa decreased the activation of astrocytes and microglia, markedly reduced levels of the pro-inflammatory cytokines IL-1β and TNF-α and increased the levels of the anti-inflammatory cytokine IL-10. Dihexa activated the PI3K/AKT signaling pathway, while PI3K inhibitor wortmannin significantly reversed the anti-inflammatory and anti-apoptotic effects of APP/PS1 mice. These findings highlight the brain AngIV/PI3K/AKT axis as a potential target for the treatment of AD.

scholarly journals PO-163 Aerobic exercise activates myocardial FGF21/FGFR1/PI3K-AKT signaling pathway and inhibits cardiomyocyte apoptosis in post-myocardial infarction rats

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Mingxiao Li ◽  
Zhenjun Tian
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Aerobic Exercise ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Collagen Fibers ◽  
Cardiomyocyte Apoptosis ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Myocardial Apoptosis

Objective To investigate the effect of aerobic exercise on the expression of fibroblast growth factor 21 (FGF21) and cardiomyocyte apoptosis in Myocardial Infarction (MI) rats. Methods male SD rats were randomly divided into three groups：the sham operation (S), sedentary MI group (MI) and MI with aerobic exercise group (ME). The MI model was established by ligation of the left anterior descending branch of the left coronary artery. ME group were trained four weeks after the operation. LVSP, LVEDP and ±dp/dtmax were used to evaluate cardiac function. H9C2 cardiomyocytes were stimulated by 400 μmol/L H2O2 for 4h to simulate myocardial apoptosis mode. AMPK agonist AICAR and FGF21 receptor inhibitor PD166866 were used to interfere with H9C2. Myocardial collagen volume fraction was calculated by Masson staining and myocardium FGF21, FGFR1, Bax, Bcl-2 and PI3K-AKT pathway by western blotting or RT-Qpcr. Cardiomyocytes apoptosis was evaluated by TUNEL. Results Compared with S, the expression of FGF21, FGFR1, Bax, Bcl-2 and PI3K, AKT increased significantly in MI group, the apoptotic cardiomyocytes and collagen fibers increased significantly, but the cardiac function decreased. Compared to MI, myocardium FGF21, FGFR1 and PI3K, AKT were further increased in ME group, the Bax/Bcl-2 and the apoptotic cardiomyocytes decreased significantly. The percentage of collagen fibers decreased and the cardiac function was improved. Myocardium FGF21 was positively correlated with the inhibition of cardiomyocyte apoptosis and the improvement of cardiac function. Furthermore, the expression of Bax/Bcl-2, TNF-α/IL-10 and the apoptotic cardiomyocytes was significantly increased by PD166866, but PI3K-AKT pathway decreased significantly by PD166866. However, AICAR single intervention or PD166866 simultaneous intervention also can reverse this adverse effects. Conclusions Exercise can increase myocardial FGF21/FGFR1 with MI. The one of the mechanisms is to activate PI3K-AKT pathway to inhibit cardiaomyocyte apoptosis and inflammatory. It indicates that FGF21/FGFR1/PI3K-AKT signaling pathway plays an important role in inhibiting myocardial apoptosis and improving cardiac function.

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