Our findings suggest that GSPE may be a novel protective agent against testicular toxicity induced by CIS.Ītherosclerosis is a complex pathology that involves both metabolic dysfunction and chronic inflammatory process. This toxicity was attenuated by GSPE treatment via activated PI3K/Akt/mTOR pathway, and inhibiting Bad/CytC/caspase-9/caspase-3 as well as PREK/eIF2α, IRE1α/XBP-1S/caspase-12 pathways. Our results indicated that CIS caused testicular toxicity via PI3K/AKT/mTOR and ERS mediated apoptosis pathway in rats. In present study, we explored the regulatory effects of GSPE on the apoptosis induced by CIS, which involved testicular apoptosis mechanisms in rats. Grape seed proanthocyanidin extract (GSPE) has been reported to serve as one of the most therapeutic potentials agents. Testicular toxicity was a well-known adverse effect of cisplatin (CIS) in cancer treatment. In conclusion, the evidence suggested that GSPE can act as a protective agent against testicular toxicity induced by CIS. And GSPE relieved endoplasmic reticulum stress-mediated apoptosis via inhibiting PREK/eIF2α and IRE1α/XBP-1S/caspase-12 pathways. These results indicated that GSPE can improve CIS-induced testicular cells apoptosis via activating PI3K/Akt/mTOR and inhibiting Bad/Cyt c/caspase-9/caspase-3 pathways. Besides, GSPE reversed the downregulation of PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR protein expression induced by CIS. The results showed that GSPE ameliorated CIS-induced the apoptosis of testicular cells and inhibited the protein levels of Bad, Cyt c, caspase-9, caspase-3, caspase-12, GRP78, CHOP, IRE1α, p-IRE1α, XBP-1S, PERK, p-PERK, eIF2α, and p-eIF2α. In this study, we aimed to investigate whether GSPE can reduce CIS-induced testicular toxicity and its potential mechanism in rats. However, the protective mechanism of GSPE against CIS-induced testicular toxicity remains unknown. Our previous study found that grape seed proanthocyanidin extract (GSPE) had a protective effect on CIS-induced testicular toxicity. Testicular toxicity is an adverse reaction of the effective chemotherapy drug cisplatin (CIS). The findings are expected to provide a theoretical basis for the clinical treatment and pathological mechanism research of AS. This study aimed to analyze the characteristics of the PI3K/Akt signaling pathway and its role in the pathogenesis of AS, as well as the role of Chinese medicine in regulating the PI3K/Akt signaling pathway. Also, the research of TCM regulation of AS via the PI3K/Akt signaling pathway has achieved certain results. In recent years, traditional Chinese medicine (TCM) has been widely recognized for its advantages of fewer side effects, multiple pathways, and multiple targets. In addition, the PI3K/Akt signaling pathway can regulate the polarization and survival of macrophages and the expression of inflammatory factors and platelet function, thus influencing the progression of AS. Stimulating and activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway can regulate the expression of vascular endothelial cytokines, thus affecting the occurrence and development of AS. Vascular endothelial injury is the initial stage of atherosclerosis (AS). This paper reviewed the mechanisms of mitochondrial dynamics and mitophagy (focus on MFN1, MFN2, OPA1, DRP1, and PINK1 proteins) and their roles in diabetic cardiomyopathy, myocardial infarction, cardiac hypertrophy, heart failure, atherosclerosis, and obesity. Cardiometabolic disease is closely related to mitochondrial dynamics and mitophagy. Cardiometabolic disease is characterized by mitochondrial dysfunction, high production of reactive oxygen species, increased inflammatory response, and low levels of ATP. Mitophagy is a process of selective removal of excess or damaged mitochondria that helps improve energy metabolism. Fission increases the number of mitochondria to ensure that they are passed on to their offspring during mitosis. Fusion allows organelles to share metabolites, proteins, and mitochondrial DNA, promoting complementarity between damaged mitochondria. Mitochondrial dynamics (fusion and fission) and mitophagy, are critical to mitochondrial function. Mitochondria play a key role in cellular metabolism.
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