Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death viaPI3K/AKT/PTENsignaling

Abstract

Cadmium (Cd) is an environmental pollutant that has an enormous influence on agricultural production, but selenium (Se) can alleviate its toxicity. The present study aimed to illustrate the effects of Se on Cd-induced heart injury. All 40 rabbits were randomly divided into four groups: control group, Se [0.5 mg kg À1 Ábody weight (BW)] group, Cd (1 mg kg À1 ÁBW) group, and Se + Cd group. After 30 days of feeding, morphological changes, the levels of oxidative stress and myocardial enzyme, the content of cardiac troponin T, programmed cell death (pyroptosis, autophagy and apoptosis), and PI3K/AKT/PTEN transduction capacity were observed. The results showed that Cd destroyed the physiological balance of trace elements and caused myocardial damage, increased the cardiac oxidative damage and led to programmed cell death.Coadministration of Se prominently ameliorated histological lesions and improved cardiac function of hearts in Cd-induced rabbits. Furthermore, Se exerted detoxification and oxidation resistance, maintained trace element homeostasis, and alleviated the changes of mRNA and protein levels of pyroptosis-, autophagy-and apoptosiscontrolling factors and PI3K/AKT/PTEN signal molecules caused by Cd. In conclusion, Se might protect against Cd-induced pyroptosis, autophagy and apoptosis by interfering with PI3K/AKT/PTEN signaling in heart.

Enhancement of cardiac angiogenesis in a myocardial infarction rat model using selenium alone and in combination with PTXF: the role of Akt/HIF-1α signaling pathway

“…Previous studies had shown the antioxidant effects of Se in ISP-induced MI in rats and in cadmium-induced cardiotoxicity in rabbits (Al-Rasheed et al 2013 ; Feng et al 2022 ). Selenium is thought to be one of the cornerstones of the body’s antioxidant defense system (Heyland et al 2005 ; Tinggi 2008 ).…”

LncRNA Miat knockdown protects against pirarubicin‐induced cardiotoxicity by targeting miRNA‐129‐1‐3p

“…Inspired by this, we overexpressed/silenced Miat and miR‐129‐1‐3p in HL‐1 and explored the function and mechanism of action of Miat. The most obvious manifestation of cardiotoxicity is the apoptosis of cardiomyocytes, and how to inhibit cardiomyocyte apoptosis is the key to attenuate cardiotoxicity 27–35 . Anthracyclines are no exception 36–38 .…”

“…The most obvious manifestation of cardiotoxicity is the apoptosis of cardiomyocytes, and how to inhibit cardiomyocyte apoptosis is the key to attenuate cardiotoxicity. [27][28][29][30][31][32][33][34][35] Anthracyclines are no exception. [36][37][38] Oxidative damage is also an important manifestation of cardiotoxicity.…”

Metal-Binding Proteins Cross-Linking with Endoplasmic Reticulum Stress in Cardiovascular Diseases

“…Lu et al [32] SelK overexpression attenuates intracellular reactive oxygen species levels and protects cells from oxidative stress-induced toxicity in cardiomyocytes Meiler et al [33] SelK enhances the expression and distribution of CD36 on the plasma membrane. SelK deficiency can reduce LDL uptake and foam cell formation, promote foam cell formation, and promote the occurrence of atherosclerosis Lewis et al [34] Macrophages, α-smooth muscle actin, RAGE receptors, VCAM-1, and CTGF are increased and atherosclerotic lesions are increased in diabetic mice lacking GPx1 and ApoE Feng et al [35] heavy metal toxicity (cadmium) Selenium inhibits oxidative stress and programmed cell death via PI3K/AKT/PTEN signaling pathway…”