prostatic hyperplasia, characterized by progressive hyperplasia of glandular and stromal tissues, is the most common proliferative abnormality of the prostate in aging men. A high-fat diet (HfD) usually is a major factor inducing oxidative stress, inflammation, and an abnormal state of the prostate. Mangosteen pericarp powder (Mpp) has abundant xanthones which can be antioxidant, anti-inflammatory, and antiproliferative agents. Therefore, the purpose of this study was to research whether MPP supplementation can affect the progression of prostatic hyperplasia. Twenty-four male F344 rats were randomly divided into four groups, including a control group (C), prostatic hyperplasiainduced group (p), prostatic hyperplasia-induced with low-dose Mpp group (pL), and induced with high-dose Mpp group (pH). the p, pL, and pH groups were given weekly intraperitoneal injections of 3,2′-dimethyl-4-aminobiphenyl (DMAB) at 25 mg/kg body weight for 10 weeks, and simultaneously fed an HFD for 24 weeks. Our findings first demonstrated that MPP consumption significantly decreased the prostate weight, serum testosterone and dihydrotestosterone concentrations, protein expression of proliferating cell nuclear antigen, and malondialdehyde levels and ameliorated mitochondrial function in prostatic tissues. these results suggest that Mpp supplementation could be used to attenuate the progression of prostatic hyperplasia. Prostatic hyperplasia is a common urologic disease that mostly affects elderly men, and it is classified as benign prostatic hyperplasia (BPH) or prostate cancer based on its severity. BPH, characterized by progressive hyperplasia of glandular and stromal tissues, is the most common proliferative abnormality of the prostate in aging men. Although research indicated that the prostate size is positively associated with increasing age 1 , pathologically, BPH presents as enlarged epithelial cells and stromal cells in the prostate. Prostatic hyperplasia has negative impacts on a patient's quality of life because prostatic hyperplasia usually induces lower urinary tract symptoms, including increased frequency of urination, increased urgency of urination, painful urination, and excessive passage of urine at night 2,3. Several factors were suggested to be associated with prostatic hyperplasia development, including oxidative stress 4-6 , inflammatory mediators 7-9 , and androgens whose abnormally increased levels can cause increased oxidative stress and immoderate expressions of growth factors which play crucial roles in the progression of prostatic hyperplasia 10-12. Oxidative stress is a cellular condition which occurs when there is an imbalance between the production and clearance of reactive oxygen species (ROS). In addition, mitochondrial DNA (mtDNA) mutations may inhibit oxidative phosphorylation, increase ROS generation, and thus lead to cell proliferation and tumor growth of the prostate gland 13. The probability of mtDNA mutations in the prostate gland increase as people get older 14. In addition, consumption of a high-fa...
BackgroundMyocardial ischemia/reperfusion (I/R) injury is one of the most important reasons for death of coronary heart disease after vascular recanalization. New evidences have shown that β2-glycoprotein I (β2GPI) plays a protective role in cardiovascular diseases. This study aims to evaluate the effects of reduced β2GPI (R-β2GPI), one form of β2GPI, on myocardial I/R injury, and to explore related mechanisms. MethodsThe in vivo myocardial I/R models of Sprague Dawley rats and in vitro hypoxia/reoxygenation(H/R) models of H9c2 cells were established. The myocardial infarction and morphological changes in SD rats were measured by the TTC staining and HE staining. Creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) levels in plasma were detected by ELISA Assay kit. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) method and caspase-3 colorimetric assay kit were used to determine myocardial apoptosis. Intracellular reactive oxygen species (ROS) generation and mitochondrial membrane potential of H9c2 cells were measured by fluorescent probe DCFH-DA and JC-1 fluorescent staining respectively. To evaluate cell damage, cell viability was assessed by determining the release of lactate dehydrogenase (LDH). The ratio of Bcl-2/Bax at mRNA level was detected by reverse transcription-polymerase chain reaction (RT-PCR). Western blot analysis was used to detect the expression levels of total Akt and phosphorylated Akt as well as the expression levels of total GSK-3βand phosphorylated GSK-3β in H9c2 cells. ResultsOur results suggested that R-β2GPI improved I/R model rats’ heart function, decreased infarct size, reduced serum CK-MB, cTnI levels, cell apoptosis and caspase3 activity. In vitro, R-β2GPI decreased LDH leakage, reduced ROS generation, maintained mitochondrial membrane potential and increased bcl-2/bax mRNA ratio; increased phosphorylation of Akt and GSK-3β in H9c2 cells following Hypoxia/Reoxygenation (H/R) jnjury. ConclusionR-β2GPI alleviated myocardial I/R (or H/R) injury by reducing oxidative stress and inhibiting mitochondrial apoptotic pathway via increasing the phosphorylation of Akt/GSK-3β.
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