scholarly journals Curcumin Synergistically Enhances the Cytotoxicity of Arsenic Trioxide in U266 Cells by Increasing Arsenic Uptake

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Dingding Han ◽  
Guibo Ma ◽  
Yujuan Gao ◽  
Yanhua Su
Keyword(s):  
Arsenic Trioxide ◽  
Western Blotting ◽  
Caspase 3 ◽  
Control Group ◽  
Arsenic Content ◽  
Dependent Manner ◽  
Arsenic Uptake ◽  
Expression Levels ◽  
Protein Levels ◽  
Drug Concentrations

Despite the constant emergence of new methods for the treatment of multiple myeloma (MM), relapse and drug resistance still exist, especially in MM with p53 mutations. Arsenic trioxide (ATO) can be used in MM treatment, but this single drug has poor effectiveness and also side effects. Curcumin is a safe and effective compound that can enhance the anticancer effects of many drugs. Previous studies have suggested that tumor cell sensitivity to ATO is related to the intracellular arsenic content, and aquaporin 9 (AQP9) is the key factor that determines intracellular arsenic content. This study aimed to explore whether curcumin can increase ATO cytotoxicity in MM and whether the mechanism is related to the regulation of intracellular arsenic content. U266 was treated with ATO, curcumin, and their combination, and cell proliferation, apoptosis, and intracellular arsenic content were detected by CCK-8 assay, flow cytometry, and HPLC-ICP-MS, respectively. AQP9 mRNA and protein levels were detected by qPCR and western blotting. The levels of Mcl-1, Bcl-2, Bax, caspase-3, and cleaved caspase-3 protein were detected by western blotting. ATO-induced cytotoxicity to U266 occurred in a time- and dose-dependent manner, but the therapeutic efficacy at low drug concentrations was modest. The arsenic content in U266 was lower than that in NB4, and the arsenic uptake by U266 was concentration-dependent. The expression levels of AQP9 mRNA and AQP9 protein in U266 were lower than those in NB4. Curcumin significantly enhanced the lethality of ATO to U266. The arsenic content in U266 in the combined drug group increased significantly compared with ATO treatment alone. After curcumin treatment, the AQP9 mRNA and AQP9 protein expression levels in U266 also increased. Compared with the control group, the expression of antiapoptotic proteins Mcl-1 and Bcl-2 decreased, the expression of proapoptotic protein Bax increased, the ratio of Bax/Bcl-2 increased, and the expression of caspase-3 decreased and cleaved caspase-3 increased in the combined drug groups. Curcumin can enhance the killing effects of ATO on U266 by increasing the intracellular arsenic content, which may be related to the upregulation of AQP9 expression. The combination of these two drugs is expected to be a potential clinical treatment for MM.

scholarly journals Decreased Endometrial IL-10 Impairs Endometrial Receptivity by Downregulating HOXA10 Expression in Women with Adenomyosis

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Junxia Wang ◽  
Chenyang Huang ◽  
Ruiwei Jiang ◽  
Yali Du ◽  
Jianjun Zhou ◽  
...  
Keyword(s):  
Western Blotting ◽  
Embryo Implantation ◽  
Control Group ◽  
Bewo Cell ◽  
Dependent Manner ◽  
Expression Levels ◽  
Positive Correlation ◽  
Protein Levels ◽  
Stat3 Phosphorylation ◽  
Ishikawa Cells

Objective. The aim of this study was to investigate the potential role of IL-10 in regulating the receptivity marker HOXA10 in the endometrium of women with adenomyosis. Methods. The expression levels of IL-10, HOXA-10, STAT3, and p-STAT3 in the endometrium of women with adenomyosis and controls were examined by means of western blotting and immunohistochemistry. The expression of the HOXA10 protein in Ishikawa cells treated with rIL-10 was examined by western blotting. The attachment rate of BeWo cell spheroids to Ishikawa cells treated with rIL-10 was expressed as a percentage of the total number of spheroids. Results. The expression levels of HOXA10 and IL-10 in the adenomyosis group were significantly lower than those in the control group, and there was a positive correlation between HOXA10 and IL-10 protein levels in all the women examined. rIL-10 increased HOXA10 expression in a concentration- and time-dependent manner by inducing the phosphorylation of STAT3 in Ishikawa cells. Treatment with rIL-10 promoted the attachment of BeWo spheroids to Ishikawa cells, which was reversed by the inhibition of STAT3 phosphorylation. The expression of p-STAT3 in the adenomyosis group was significantly lower than that in the control group, and there was a positive correlation between IL-10 and p-STAT3 protein levels in all the women examined. Conclusions. Both IL-10 and HOXA10 levels in the endometrium are significantly reduced in women with adenomyosis compared with those in control women. The phosphorylation of STAT3 has been proven to be a critical mediator between IL-10 and HOXA10, which may play critical roles in embryo implantation.

Biological and Molecular Evidences for the Antitumor and Antioxidant Potential of Quercetin In Vitro

2020 ◽  
Vol 14 (4) ◽  
pp. 499-505
Author(s):  
Jia Zhou ◽  
Yan Xu ◽  
He Lin ◽  
Guangfu Lv ◽  
Ying Chen ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Hela Cell ◽  
Western Blotting ◽  
Hela Cells ◽  
Caspase 3 ◽  
Umbilical Vein ◽  
Expression Level ◽  
Dependent Manner ◽  
Expression Levels ◽  
Apoptosis Rate

To investigate the protective mechanisms of quercetin in promoting HeLa cell apoptosis and protecting human umbilical vein endothelial cells (HUVECs) from oxidative damage, in this study, MTT test was preformed to observe the inhibition rate of quercetin on HeLa cell proliferation (50.0, 75.0 and 100.0 mol/L), and the apoptosis rate was measured with flow cytometry. Western blotting was used to detect the protein expression levels in signaling pathways in quercetin-treated HeLa cells and HUVECs. MTT assay results showed that quercetin could inhibit (P < 0.001) the proliferation of HeLa cells in a time-concentration dependent manner. Apoptosis results showed that quercetin can increase the early and late apoptosis rate (P < 0.001). Western blotting revealed that quercetin can down-regulate BCL-2 expression level (P < 0.05), up-regulate BAX and CASPASE-3 expression level (P < 0.05) in HeLa cells. Flow detection results showed that the number of HUVECs labeled with CD105/CD62E and CD31/CD34 in the oxidation group decreased significantly (P < 0.01), increased significantly (P < 0.001) in the drug group. Quercetin can decrease the expression levels of p16, p53 and p21 significantly (P < 0.05). In conclusion, quercetin can promote the apoptosis of HeLa cell by regulating the expression level of CASPASE-3, BCL-2 and BAX; and protect HUVECs against oxidative damage and inhibit the apoptosis by down-regulating p16, p53 and p21.

scholarly journals Inhibitory Effect of Centipede Scolopendra Extract on Gallbladder Carcinoma via Up-regulation of PUMA

2021 ◽  
Author(s):  
Cheng Yan ◽  
Yangyan Xiao ◽  
Jingfen Ji ◽  
Zhide Liu ◽  
Weichang Zhang ◽  
...  
Keyword(s):  
Cell Line ◽  
Western Blotting ◽  
Gallbladder Carcinoma ◽  
Colony Formation ◽  
Control Group ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
Sirna Group

Abstract Background: To observe the effect of centipede scolopendra extract on gallbladder carcinoma (GBC) and further investigate its underlying mechanism.Methods: The GBC cell line GBC-SD was purchased and cultured. Small interfering RNA (siRNA) was constructed. The mRNA expression levels of PUMA were measured by reverse transcription-quantitative PCR (RT-qPCR) and protein expression levels of p53, PUMA, Bax and Bcl-2 were measured by western blotting respectively. Viability and proliferation were detected using MTT and colony formation assays respectively. The apoptosis rate was determined by Annexin-V-FITC/PI double staining. Results: The GBC-SD cell line was successfully obtained and cultured. MTT and colony formation assays demonstrated that the viability and proliferation of GBC-SD cells could be markedly inhibited by centipede scolopendra extract in a concentration-dependent manner in the limited concentration range. Following pretreatment with centipede scolopendra extract, RT-qPCR demonstrated that the expression levels of PUMA were markedly increased in the GBC-SD cells, and western blotting showed that the high expression of PUMA was accompanied by upregulation of Bax and downregulation of p53 and Bcl-2 in the GBC-SD cells. However, this effect has proved hard to reproduce after PUMA-siRNA. Flow cytometry revealed that the apoptosis rate was 9.8±2.2%, 25.3±3.6%, 10.6±2.0%, and 13.5±2.4% in control group, centipede scolopendra extract group, PUMA-siRNA group, and centipede scolopendra extract combined with PUMA-siRNA group respectively. Conclusions: Centipede scolopendra extract could induce the apoptosis of GBC-SD cells by promoting the PUMA-Bax signaling pathway. It could serve as a potential novel therapy for GBC in clinical practice.

scholarly journals Silencing of Vangl2 attenuates the inflammation promoted by Wnt5a via MAPK and NF-κB pathway in chondrocytes

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Ke Zhang ◽  
Zhuoying Li ◽  
Yunyang Lu ◽  
Linyi Xiang ◽  
Jiadong Sun ◽  
...  
Keyword(s):  
Western Blotting ◽  
Planar Cell Polarity ◽  
Type Ii Collagen ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Inflammatory Microenvironment ◽  
Functional Roles ◽  
Protein Levels ◽  
Oa Chondrocytes

Abstract Background The Wnt planar cell polarity (PCP) pathway is implicated in osteoarthritis (OA) both in animals and in humans. Van Gogh-like 2 (Vangl2) is a key PCP protein that is required for the orientation and alignment of chondrocytes in the growth plate. However, its functional roles in OA still remain undefined. Here, we explored the effects of Vangl2 on OA chondrocyte in vitro and further elucidated the molecular mechanism of silencing Vangl2 in Wnt5a-overexpressing OA chondrocytes. Methods Chondrocytes were treated with IL-1β (10 ng/mL) to simulate the inflammatory microenvironment of OA. The expression levels of Vangl2, Wnt5a, MMPs, and related proinflammatory cytokines were measured by RT-qPCR. Small interfering RNA (siRNA) of Vangl2 and the plasmid targeting Wnt5a were constructed and transfected into ATDC5 cells. Then, the functional roles of silencing Vangl2 in the OA chondrocytes were investigated by Western blotting, RT-qPCR, and immunocytochemistry (ICC). Transfected OA chondrocytes were subjected to Western blotting to analyze the relationship between Vangl2 and related signaling pathways. Results IL-1β induced the production of Vangl2, Wnt5a, and MMPs in a time-dependent manner and the significantly increased expression of Vangl2. Vangl2 silencing effectively suppressed the expression of MMP3, MMP9, MMP13, and IL-6 at both gene and protein levels and upregulated the expression of type II collagen and aggrecan. Moreover, knockdown of Vangl2 inhibited the phosphorylation of MAPK signaling molecules (P38, ERK, and JNK) and P65 in Wnt5a-overexpressing OA chondrocytes. Conclusions For the first time, we demonstrate that Vangl2 is involved in the OA process. Vangl2 silencing can notably alleviate OA progression in vitro by inhibiting the expression of MMPs and increasing the formation of the cartilage matrix and can inhibit the proinflammatory effects of Wnt5a via MAPK and NF-κB pathway. This study provides new insight into the mechanism of cartilage inflammation.

scholarly journals Perfluorooctanoic Acid Exposure in Early Pregnancy Induces Oxidative Stress in The Uterus and Liver in Mice

2021 ◽  
Author(s):  
Yan Zhang ◽  
Linchao Zhang ◽  
JiaLu Bao ◽  
LianTao Liu ◽  
Xiaodan Wang
Keyword(s):  
Early Pregnancy ◽  
Caspase 3 ◽  
Liver Toxicity ◽  
Liver Weight ◽  
Perfluorooctanoic Acid ◽  
Control Group ◽  
Dependent Manner ◽  
Subsequent Increase ◽  
Decidual Cells ◽  
Pregnant Mice

Abstract To investigate the mechanism perfluorooctanoic acid (PFOA)’s toxicity on the uterus and liver of the mice during early pregnancy, pregnant mice were given 0, 1, 5, 10, 20, 40 mg/kg PFOA daily by gavage from gestational day (GD) 1-7, and sacrificed on GD 9. Uterus and liver weight were recorded, liver and uterine indexes were calculated, histopathological changes of the liver and uterus were examined, and levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) in liver were detected by spectrophotometric method. Expression of FAS, FASL, Bax, Bcl-2, and Caspase-3 in decidual cells were detected by immunohistochemistry and the TUNEL method was used to detect apoptotic uterine cells. Results showed that liver weight increased, and the uterus index was significantly reduced at 40 mg/kg compared with the control group. With increasing doses of PFOA, levels of SOD and GSH-PX were significantly decreased, and MDA significantly increased in liver tissue. 20 mg/kg and 40 mg/kg of PFOA caused greater harm to the uterus and congestion and resorption may occur. Expression of FAS, FASL, Bax, and Caspase-3 in decidual cells of the uterus in PFOA treatment groups significantly increased in a dose-dependent manner. The expression of Bcl-2 was down-regulated, which decreased the ratio of Bcl-2/Bax. It is therefore proposed that oxidative damage may be one of the mechanisms by which PFOA induces liver toxicity, and a subsequent increase in uterine cell apoptosis may induce embryo loss or damage.

scholarly journals Expression levels of caspase-3 and gasdermin E and their involvement in the occurrence and prognosis of lung cancer

2021 ◽  
Author(s):  
yuanli huang ◽  
GuangHui Zhang ◽  
Qing Zhu ◽  
Xia Wu ◽  
LIGao Wu
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Clinical Stage ◽  
The Body ◽  
Caspase 8 ◽  
Survival Prognosis ◽  
Expression Levels ◽  
Protein Levels ◽  
Normal Tissues ◽  
Related Proteins

Abstract Background Pyroptosis plays a dual role in the development of cancer and malignancy, and as such, may potentially be a new target for cancer treatment. However, the inflammatory response to pyroptosis may have adverse effects on the body. The roles of gasdermin E (GSDME), caspases, and related proteins associated with pyroptosis in cancer remain controversial. This study aimed to explore whether the expression levels of caspase-3 and GSDME affect the clinical stage, pathological grade, and survival prognosis of patients with lung cancer. Methods We examined the protein levels of GSDME, caspase-3, caspase-8, and caspase-9 in lung tissues from 100 patients with lung cancer by using immunohistochemistry. Results We found that GSDME, caspase-3, and caspase-8 were more highly expressed in the tumor tissues than in the adjacent normal tissues. Moreover, we found that GSDME could serve as a prognostic factor because there was a positive correlation between its expression level and the postoperative survival rate of patients with lung cancer. Conclusions GSDME may be an independent factor affecting the prognosis of patients with lung cancer. However, the role of GSDME and its related proteins in cancer requires further research.

ATI-2341 Trifluoroacetic Acid (TFA) Promotes Menstrual Blood-Derived Mesenchymal Stem Cell Recruitment and Enhances Uterine Repair Through Gi Pathway in Asherman’s Syndrome

2022 ◽  
Vol 12 (3) ◽  
pp. 506-513
Author(s):  
Ying Lv ◽  
Liyan Ye ◽  
Xiujuan Zheng
Keyword(s):  
Menstrual Blood ◽  
Control Group ◽  
Dependent Manner ◽  
Asherman’S Syndrome ◽  
Expression Levels ◽  
Endometrial Cells ◽  
Injury Model ◽  
Recruitment Effect ◽  
Dose Dependent

This study aimed to explore the role of ATI-2341 in Asherman’s syndrome and its impact on menstrual blood-derived mesenchymal stem cells (MenSCs). Following establishment of endometrial injury model, MenSCs were extracted from rats and cultured. They were treated with ATI-2341 TFA at different concentrations (10 ng/mL, 50 ng/mL, 100 ng/mL) and MenSCs treated without ATI-2341 TFA were taken as controls. Flow cytometry was conducted to detect the cell cycle. MTT was carried out to evaluate proliferation of endometrial cells. The expression levels of MMP-9, TIMP-1, CK, and VIM were determined with staining used to reflect morphology of endometrium. Administration with ATI-2341 TFA resulted in decreased expression of MMP-9 and increased expression of TIMP-1 in a dose-dependent manner. Of note, the increase of ATI-2341 TFA concentration was accompanied with elevated cell proliferation rate, increased number of glands in the endometrium, and decreased fibrosis area. As treated with 100 ng/mL ATI-2341 TFA, the cells exhibited more glands than that under other concentrations with uniformly arranged glands and lowest expression levels of CK and VIM, control group had plenty of blue-stained collagen fibers in the intima and least amount of glands. ATI-2341 TFA 100 ng/mL induced endometrial epithelial recruitment effect on MenSCs and promoted endometrial repair more significantly than Gi-3 pathway agonists. Collectively, ATI-2341 TFA enhances MenSC recruitment and facilitates endometrial epithelial cells proliferation and the repair of uterine damage in Asherman’s syndrome through Gi pathway. These findings provide a\ novel insight into the MenSC-based treatment against Asherman’s syndrome and deserve further investigation.

The Warburg effect promoted the activation of the NLRP3 inflammasome induced by Ni-refining fumes in BEAS-2B cells

2020 ◽  
Vol 36 (8) ◽  
pp. 580-590
Author(s):  
Rui Wang ◽  
Sheng-Yuan Wang ◽  
Yue Wang ◽  
Rui Xin ◽  
Bing Xia ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Warburg Effect ◽  
Hypoxia Inducible Factor ◽  
Lactate Production ◽  
Control Group ◽  
Dependent Manner ◽  
Chain Reactions ◽  
Protein Levels ◽  
Polymerase Chain Reactions ◽  
The Warburg Effect

Nickel (Ni) is a known human carcinogen that has an adverse effect on various human organs in occupational workers during Ni refinement and smelting. In the present study, we used real-time polymerase chain reactions, Western blot analysis, and a lactate production assay to investigate whether an increase in the NLRP3 inflammasome induced by Ni-refining fumes was associated with the Warburg effect in BEAS-2B cells, a nonmalignant pulmonary epithelial line. Exposure to Ni-refining fumes suppressed cell proliferation and increased lactate production compared with those in an untreated control group in a dose- and time-dependent manner. Ni-refining fumes induced the Warburg effect, which was observed based on increases in the levels of hypoxia-inducible factor-1α, hexokinase 2, pyruvate kinase isozyme type M2, and lactate dehydrogenase A. In addition, Ni-refining fumes promoted increased expression of NLRP3 at both the gene and protein levels. Furthermore, inhibition of the Warburg effect by 2-Deoxy-d-glucose reversed the increased expression of NLRP3 induced by Ni-refining fumes. Collectively, our data demonstrated that the Warburg effect can promote the expression of the NLRP3 inflammasome induced by the Ni-refining fumes in BEAS-2B cells. This indicates a new phenomenon in which alterations in energy production in human cells induced by Ni-refining fumes regulate the inflammatory response.

scholarly journals Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Yongpan Huang ◽  
Xinliang Li ◽  
Xi Zhang ◽  
Jiayu Tang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Brain Injury ◽  
Western Blotting ◽  
Caspase 3 ◽  
Memory Function ◽  
Diabetic Rats ◽  
Oxygen Species ◽  
Expression Levels

Oxymatrine (OMT) is the major quinolizidine alkaloid extracted from the root of Sophora flavescens Ait and has been shown to exhibit a diverse range of pharmacological properties. The aim of the present study was to investigate the role of OMT in diabetic brain injury in vivo and in vitro. Diabetic rats were induced by intraperitoneal injection of a single dose of 65 mg/kg streptozotocin (STZ) and fed a high-fat and high-cholesterol diet. Memory function was assessed using a Morris water maze test. A SH-SY5Y cell injury model was induced by incubation with glucose (30 mM/l) to simulate damage in vitro. The serum fasting blood glucose, insulin, serum S100B, malondialdehyde (MDA), and superoxide dismutase (SOD) levels were analyzed using commercial kits. Morphological changes were observed using Nissl staining and electron microscopy. Cell apoptosis was assessed using Hoechst staining and TUNEL staining. NADPH oxidase (NOX) and caspase-3 activities were determined. The effects of NOX2 and NOX4 knockdown were assessed using small interfering RNA. The expression levels of NOX1, NOX2, and NOX4 were detected using reverse transcription-quantitative PCR and western blotting, and the levels of caspase-3 were detected using western blotting. The diabetic rats exhibited significantly increased plasma glucose, insulin, reactive oxygen species (ROS), S-100B, and MDA levels and decreased SOD levels. Memory function was determined by assessing the percentage of time spent in the target quadrant, the number of times the platform was crossed, escape latency, and mean path length and was found to be significantly reduced in the diabetic rats. Hyperglycemia resulted in notable brain injury, including histological changes and apoptosis in the cortex and hippocampus. The expression levels of NOX2 and NOX4 were significantly upregulated at the protein and mRNA levels, and NOX1 expression was not altered in the diabetic rats. NOX and caspase-3 activities were increased, and caspase-3 expression was upregulated in the brain tissue of diabetic rats. OMT treatment dose-dependently reversed behavioral, biochemical, and molecular changes in the diabetic rats. In vitro, high glucose resulted in increases in reactive oxygen species (ROS), MDA levels, apoptosis, and the expressions of NOX2, NOX4, and caspase-3. siRNA-mediated knockdown of NOX2 and NOX4 decreased NOX2 and NOX4 expression levels, respectively, and reduced ROS levels and apoptosis. The results of the present study suggest that OMT alleviates diabetes-associated cognitive decline, oxidative stress, and apoptosis via NOX2 and NOX4 inhibition.

Effects of Hydrogen-rich Water on the PI3K/AKT Signaling Pathway in Rats with Myocardial Ischemia-reperfusion Injury

2020 ◽  
Vol 20 (5) ◽  
pp. 396-406 ◽  
Author(s):  
Liangtong Li ◽  
Xiangzi Li ◽  
Zhe Zhang ◽  
Li Liu ◽  
Tongtong Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
Water Group

Background: The effects of hydrogen-rich water on PI3K/AKT-mediated apoptosis were studied in rats subjected to myocardial ischemia-reperfusion injury (MIRI). Methdos: Sixty rats were divided randomly into a hydrogen-rich water group and a control group. The hearts were removed and fixed in a Langendorff device. Hearts from the control group were perfused with K-R solution, and hearts from the hydrogen-rich water group was perfused with K-R solution + hydrogen-rich water. The two treatment groups were then divided randomly into pre-ischemic period, ischemic period and reperfusion period groups(10 rats per group), which were subjected to reverse perfusion for 10 min, normal treatment for 20 min, and reperfusion for 20 min, respectively. The mRNA and protein expression levels of PI3K, AKT, p-AKT, FoxO1, Bim and Caspase-3 in each group were detected by RT-qPCR, immunohistochemistry (IHC) and Western blotting. Caspase-3 activity was detected by spectrophotometry. Results: Among the hydrogen-rich water group, the PI3K/AKT signaling pathway was significantly activated, and FoxO1, Bim, and Caspase-3 mRNA and protein levels were significantly decreased in ischemia-reperfusion subgroup compared with the preischemic and ischemic subgroups. In the ischemia-reperfusion hydrogen-rich water group, PI3K, AKT and p-AKT mRNA and protein expression levels were increased while the FoxO1, Bim and Caspase-3 expression levels were significantly decreased compared with those in the corresponding control group (p<0.05). Conclusion: Hydrogen-rich water can activate the PI3K/AKT signaling pathway, alleviate ischemia-reperfusion injury in isolated rat hearts, and inhibit cardiomyocyte apoptosis.

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