甜瓜属线粒体基因组的父系遗传特性

为分析甜瓜属线粒体基因组的遗传特性,选取甜瓜属11个不同种植物为试验材料,采用成熟花粉DAPI压片染色方法结合树脂半薄切片MTG-DAPI双染色技术,观察花粉贴壁期和成熟期细胞中的线粒体分布。结果显示,所涉及的11种甜瓜属植物均同黄瓜一样,成熟花粉细胞生殖核周围或精细胞中存在线粒体DNA;而作为对照的南瓜和西葫芦的花粉细胞发育到成熟期时生殖核周围没有任何细胞器DNA。上述结果表明,甜瓜属植物线粒体DNA有可能通过花粉进行遗传和散布。这个结果将线粒体基因组父系遗传潜力特性扩展到甜瓜属,为进一步探究植物线粒体基因组的父系遗传机制奠定基础。     

硅对干旱胁迫下番茄根系细胞超微结构及线粒体活性氧代谢的影响

以番茄品种‘金棚1号’为试材,采用水培方法,研究了PEG-6000模拟干旱胁迫条件下,硅对根系细胞超微结构及线粒体活性氧代谢的影响。结果表明,随干旱胁迫时间的延长,番茄植株根系活力逐渐降低,丙二醛（MDA）含量逐渐升高,细胞线粒体超氧阴离子生成速率和过氧化氢（H2O2）含量亦逐渐升高,而超氧化物歧化酶（SOD）、过氧化物酶（POD）及过氧化氢酶（CAT）活性在胁迫初期迅速增强,达峰值后又快速降低;施硅处理显著抑制了干旱胁迫引发的上述变化。干旱胁迫处理12 d时,施硅较不施硅处理番茄根系的MDA含量、超氧阴离子生成速率和H2O2含量分别降低了25.14%、8.34%和20.25%,而根系活力、SOD活性、POD活性和CAT活性分别提高了139.62%、243.19%、65.53%和125.55%。施硅处理还减轻了干旱胁迫导致的根系细胞质壁分离程度,缓解了线粒体、细胞核、生物膜等的损伤。     

柑橘褐斑病菌信号转导基因及活性氧解毒机制研究进展

由链格孢菌（Alternaria alternata）引起的柑橘褐斑病（Alternaria brown spot,ABS）是严重为害柑橘的一种真菌病害。在柑橘褐斑病菌中已鉴定出多个信号转导基因,但大多围绕单基因生物学功能的研究,关于信号级联通路主要集中在病原菌解毒活性氧（reactive oxygen species,ROS）方面。研究发现除毒素ACT外,柑橘褐斑病菌对活性氧的高效解毒机制也是其致病所必需的。对柑橘褐斑病菌信号转导基因研究现状进行综述,分析其活性氧解毒相关通路及机制,旨在为进一步研究柑橘褐斑病菌分子致病机制提供参考。     

Pathogenesis,prevention and treatment of COVID-19 based on Th17/Treg immune imbalance

The extremely severe epidemic situation of coronavirus disease 2019 （COVID-19） outbreak around the world with high infectiousness and rapid spread has become a public health emergency of international concern. The disease is caused by severe acute respiratory syndrome coronavirus 2 （SARS-CoV-2）, and cytokine storm is an important pathological manifestation. Related studies have shown that cytokine storm and dysregulation of host immune responses characterized by lymphopenia are important mechanisms for the pathogenesis of severe COVID-19. The immune response disorder of COVID-19 is closely related to T helper 17 cell/regulatory T cell （Th17/Treg） immune imbalance. SARS-CoV-2 infection leads to excessive activation of lung immune cells, forming a cytokine storm dominated by interleukin-6 （IL-6）. Then, the Th17/Treg immune balance is broken, forming a vicious circle, which eventually promotes the rapid aggravation of the disease. Finally, COVID-19 progresses into acute respiratory distress syndrome, and even respiratory failure until death. Therefore, it is more important to discuss the prevention and treatment of COVID-19 from the perspective of immune imbalance. On the view of treatment, before effective antiviral drugs and vaccines are successfully developed, we should pay attention to immune regulation for severe and critically ill patients. Treatments with inflammatory factor blockers, glucocorticoids, recovered plasma and traditional Chinese medicine have certain immunomodulatory effect. This article discusses the pathogenesis of COVID-19 based on Th17/Treg immune imbalance, and elaborates on immunomodulatory therapy, aiming to provide reference for the prevention and treatment of COVID-19 and drug development.     

Role of mitochondrial dysfunction in genesis of severe shock

The high mortality is a leading element of human health that follows severe shock even after blood transfusion and other anti-shock therapy. Therefore, to find out the mechanism of high mortality in severe shock is very critical. As a hotspot in recent years, mitochondrial function has important value in the genesis of many diseases, such as cardiovascular diseases, diabetes mellitus, Alzheimer disease, Parkinson disease, nonalcoholic steatohepatitis and so on. Mitochondrial dysfunction often takes place in relation to the opening of mitochondrial permeability transition pore with intracellular low ATP content in severe shock. The consequence of intracellular low ATP content may lead to the dysfunction of various organs with difficult treatment of severe shock. Therefore, protection against mitochondrial damage is a novel approach for treatment of severe shock. This article summarizes the concept, pathogenesis, detection variables and treatment of mitochondrial dysfunction in severe shock.     

Activation of NF-κB-iNOS/COX-2 signaling pathways is involved in impaired endothelium-dependent relaxation under high glucose condition

AIM To investigate the role of nuclear factor-κB （NF-κB）-inducible nitric oxide synthase （iNOS）/cyclooxygenase-2 （COX-2） signaling pathways in impaired endothelium-dependent relaxation under high glucose （HG） condition. METHODS The endothelium-dependent relaxation induced by acetylcholine （ACh） in phenylephrine-precontracted rat thoracic aortic ring was performed in the absence or presence of different inhibitors under HG （55 mmol/L glucose） condition, and then the maximal relaxation effect of ACh （E_max） and the negative logarithm of ACh concentration for inducing 50% of E_max （pD₂） were calculated. The structure of aorta was observed by HE staining and electron microscopy. The mRNA and protein expression was detected by RT-qPCR and Western blot, respectively. RESULTS The structure of endothelial cells was interrupted by HG. Meanwhile, ACh-induced vasodilatation was also impaired, in which the E_max and pD₂ were both decreased significantly （P<0.01）, accompanied by the up-regulation of NF-κB p65, iNOS and COX-2 expression at mRNA and protein levels （P<0.01）. The NF-κB inhibitor PDTC, iNOS inhibitor SMT, and COX-2 inhibitor meloxicam restored the ACh-induced vasodilatation under HG condition, in which the E_max and pD₂ were increased significantly （P<0.01）. Moreover, PDTC attenuated the pathological damage of endothelial structure, and down-regulated the expression levels of NF-κB p65, iNOS and COX-2 induced by HG （P<0.01）. CONCLUSION The activation of NF-κB-iNOS/COX-2 signaling pathways is involved in the impaired endothelium-dependent relaxation under HG condition.     

DL-3-n-butylphthalide attenuates mitochondrial damage in vascular endothelial cells under the condition of oxygen-glucose deprivation

AIM:To investigate the mechanism in which DL-3-n-butylphthalide (NBP) protects the mitochondria from the damage of oxygen-glucose deprivation (OGD). METHODS:Human umbilical vein endothelial cells (HUVECs) were exposed to OGD to induce endothelial damage. Mitochondrial morphology and mitochondrial reactive oxygen species (ROS) were examined using MitoTracker Green and MitoSOX Red, respectively. The activity of superoxide dismutase (SOD) was evaluated by SOD assay kit. RESULTS:NBP significantly attenuated OGD-induced mitochondrial fragmentation, reduced the content of mitochondrial ROS and increased the activity of SOD. CONCLUSION:NBP alleviates OGD-induced damage in the mitochondria. Reduction of mitochondrial ROS and enhancement of SOD activity may be the mechanism in which NBP protects mitochondria.     

Quercetin activates mitochondrial autophagy via PINK1/parkin pathway to alleviate cerebral ischemia-reperfusion injury in rats

AIM To analyze the regulatory effect of quercetin （QUE） on PTEN-induced putative kinase 1 （PINK1）/parkin mitochondrial autophagy pathway, and to explore the mechanism of quercetin in relieving cerebral ischemia/reperfusion （I/R） injury. METHODS Sixty SD male rats were randomly divided into sham operation group, model group （I/R group）, QUE group,3-methyladenine （3-MA） group and QUE+3-MA group. Administration started in each group 3 days before modeling, once a day, at 30 min after the last administration,except sham group, the other groups used 4-vessel blockage method to establish the whole brain I/R model. On the day after modeling, the neural function was evaluated by neuropathy disability score （NDS）. The volume of cerebral infarction was measured by 2,3,5-triphenyltetrazolium chloride （TTC） staining. The morphological changes of mitochondria in hippocampus were observed by transmission electron microscopy. The contents of interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-α） in hippocampus were measured by ELISA. The activity of superoxide dismutase （SOD） and contents of malondialdehyde （MDA） in hippocampus were detected by xanthine oxidase method, thiobarbituric acid condensation method. Western blot was used to detect the proteinex pression of PINK1, parkin and LC3-II in brain tissue. RESULTS Compared with sham group, the hippocampus of the rats in I/R group and QUE+3-MA group showed swelling of mitochondria, destruction or disappearance of internal crista and other pathological damage,also the volume of cerebral infarction, the contents of IL-6, TNF-α and MDA, the protein expression levels of PINK1, parkin and LC3-II were increased （P<0.05）, while NDS score and activity of SOD were decreased （P<0.05）. Compared with I/R group and QUE+3-MA group, the pathological damage degree of hippocampus in QUE group was reduced, the volume of cerebral infarction, the contents of IL-6, TNF-α and MDA were decreased （P<0.05）, the proteinexpression levels of PINK1, parkin and LC3-II, and NDS score and activity of SOD were increased （P<0.05）.The above indexes in 3-MA group were opposite to QUE group. No significant difference in the above indexes between I/R group and QUE+3-MA group was observed （P>0.05）. CONCLUSION Quercetin activates mitochondrial autophagy and reduces cerebral I/R by regulating the expression of PINK1/parkin pathway proteins.     

Effects of uric acid on mitochondrial damage and Pgam5/Drp1 expression in rat kidney cells

AIM To investigate the effects of uric acid on mitochondrial damage and the expression of phosphoglycerate mutase family member 5 (Pgam5) and dynamin-related protein 1 (Drp1) in rat kidney cells. METHODS Normal rat kidney NRK-52E cells were treated with uric acid at 0.6 mmol/L. The cell viability was measured by MTT assay. The cell morphological change was observed by Hoechst 33258 staining. The apoptosis of the cells was analyzed by flow cytometry. The morphological structure of mitochondria was observed under transmission electron microscope. The expression of Pgam5 and Drp1 was examined by immunofluorescence staining. The mRNA expression of Pgam5 in mitochondria was detected by RT-qPCR. The protein expression of Pgam5 and Drp1 in the cytoplasmic matrix was determined by Western blot. RESULTS Uric acid significantly decreased the viability of NRK-52E cells, and significantly increased the apoptotic rate of the cells (P<0.01). Mitochondrial swelling, vacuolation and cristal rupture were observed after the NRK-52E cells were treated with uric acid, and the mRNA expression of Pgam5 in mitochondria was decreased significantly, while the protein expression of Pgam5 and Drp1 in the cytoplasmic matrix was increased significantly (P<0.01). CONCLUSION Uric acid intervention destroys the mitochondrial structure of rat renal cells, up-regulates the expression of Pgam5 and Drp1 in the cytoplasmic matrix, and induces apoptosis of the cells.     

Role of damaged mitochondria in Vibrio vulnificus induced dendritic cell apoptosis

AIM： To investigate the role of damaged mitochondria in dendritic cell (DC) apoptosis induced by Vibrio vulnificus (Vv) and its possible mechanism. METHODS：DC2.4 cells were co-cultured with Vv 1.1758 strain. Fluorescent probes DCFH-DA and Fluo-8-AM were used to detect reactive oxygen species (ROS) and intracellular Ca2+ concentration in the invaded cells, respectively. The cellular apoptotic rates and mitochondrial membrane potential (Δψm) were measured by flow cytometry. The expression of nuclear factor-kappa B p65 (NF-κB p65) and tumor necrosis factor-alpha (TNF-α) was detected by Western blotting. RESULTS： Vv 1.1758 induced DC2.4 cell apoptosis. Vv 1.1758 bacteria invaded into the DC2.4 cells by binding with cellular membrane though the end of the body. In the invaded DC2.4 cells, the visible mitochondrial damage, elevated ROS and intracellular Ca2+ levels, and declined Δψm were presented. After 1 h of co-culture, NF-κB p65 began to rise and reached the peak at 5 h, and then slightly decreased at 6 h. The TNF-α level increased after 2 h of co-culture and reached the peak at 6 h. CONCLUSION： The damaged mitochondria play an important role in DC apoptosis induced by Vv, and its possible mechanism may associate with the elevation of ROS and intracellular Ca2+ level, and the declined Δψm. Meanwhile, NF-κB p65 and TNF-α are potential critical signaling molecules in the process of apoptosis.     

Progress of P-selectin glycoprotein ligand-1 in kidney diseases

P-selectin glycoprotein ligand-1 (PSGL-1) is an adhesion molecule mainly expressed on the surface of leukocytes and platelets, which plays a vital part in immune recognition, inflammatory response and thrombosis. The prevalence of chronic kidney disease (CKD) is increased gradually and it has been one of major diseases that threaten the world's public health. In addition, its etiology is complicated, and most of the pathogenesis is incompletely understood. Researches show that PSGL-1 participates in the development of kidney diseases in a variety of ways, and its mechanism may involve signaling pathways such as TGF-β1/Smad and PI3K/AKT/GSK-3β, as well as key renal regulators such as connective tissue growth factor and chemokine (C-C motif) ligand 2. This review summarizes the research progress of PSGL-1 in renal fibrosis, lupus nephritis, obesity-related kidney disease and acute kidney injury.     

Cyanidin attenuates pressure overload-induced cardiac remodeling in mice via mitochondrial fusion enhancement

AIM To investigate the effect of cyanidin （Cyn） on pressure overload-induced cardiac remodeling and the underlying mechanism. METHODS Six-week-old male C57BL/6 mice （n=120） were divided into 4 groups： sham group （n=20）, sham+Cyn group （n=20）, transverse aortic constriction （TAC） group （n=40） and TAC+Cyn group （n=40）. The model of cardiac chronic pressure overload was induced by TAC, and the first day of TAC was defined as day 0. The animals in sham+Cyn group and TAC+Cyn group were treated with Cyn dissolved in DMSO and normal saline （5 mg·kg^-1·d^-1） for 5 d before TAC, while the animals in sham group and TAC group were treated with the same amount of DMSO and normal saline. Four weeks after TAC, the survival rate of the animals in each group was analyzed, the heart function of the mice was measured by ultrasound echocardiography, and the heart weight/body weight and lung weight/body weight were calculated. The cross-sectional area of the cardiomyocytes was measured by wheat germ agglutinin staining and hematoxylin-eosin staining. The degree of cardiac oxidative stress was evaluated by dihydroethidium staining and measurement of superoxide dismutase （SOD） and malondialdehyde （MDA） levels. The cardiomyocyte apoptosis was detected by TUNEL method. The mRNA expression levels of atrial natriuretic peptide （ANP）, brain natriuretic peptide （BNP） and β-myosin heavy chain （β-MHC） were detected by RT-qPCR, and the protein expression levels of Bax, Bcl-2, optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were determined by Western blot. The mitochondrial morphological changes were observed by transmission electron microscopy. RESULTS Compared with TAC group, the survival rate of the mice in TAC+Cyn group was significantly increased （P<0.05）, the myocardial apoptosis, the cross-sectional area of myocardial cells, the heart weight/body weight, the lung weight/body weight, the level of reactive oxygen species and the MDA content were decreased （P<0.05）, and the SOD was activated （P<0.05）. M-mode ultrasound tests showed that Cyn treatment significantly increased left ventricular ejection fraction and left ventricular fractional shortening in the mice after TAC （P<0.05）, while left ventricular end-diastolic diameter and left ventricular posterior wall thickness in diastole were reduced （P<0.05）. Transmission electron microscopic observation showed that the number of myocardial mitochondria was increased and the mitochondrial area was decreased after TAC （P<0.05）, while treatment with Cyn increased the area of myocardial mitochondria and decreased the mitochondrial number （P<0.05）. Compared with sham group, the protein level of OPA1 in TAC group was significantly reduced （P<0.05）, while treatment with Cyn significantly increased the protein level of OPA1. CONCLUSION Cyanidin significantly increases the survival rate, improves the cardiac function and attenuates the cardiac remodeling of the mice after TAC. The mechanism may be related to the inhibition of myocardial mitochondrial OPA1 cleavage and the promotion of mitochondrial fusion.     

Activation of repair pathways after neuronal DNA damage induced by bupivacaine

AIM To investigate the activation of related repair pathways after bupivacaine-induced neuronal DNA damage by cDNA gene screening. METHODS The bupivacaine-induced SH-SY5Y neuronal damage and DNA damage model was established. The technique of cDNA microplate array was used to screen the 21 important regulatory factors in the DNA damage repair pathway. Post-analysis of these differentially expressed repair genes for the repair pathway enrichment and distribution was performed. The data were analyzed by GraphPad Prism 6 statistical software to compare differences between groups. RESULTS The viability of SH-SY5Y cells treated with bupivacaine at different concentrations （detected by CCK-8 assay） showed that the IC₅₀ value of bupivacaine was 1.5 mmol/L. The comet assay related index （the comet tail） was increased （P<0.05）, the phosphorylation level of γH2AX protein was increased （P<0.05）, indicating that DNA damage in the SH-SY5Y cells was significantly aggravated after bupivacaine treatment. The results of cDNA microplate assay showed that compared withcontrol group, the differentially expressed genes after bupivacaine treatment were DNA-PKcs, PTEN, NTH1, RAD9, CSB, GADD45, XPD, XPC-HR23B and P53. The analysis showed that these repair genes were mainly concentrated in the following 3 repair mechanisms： base excision repair, nucleotide excision repair, and non-homologous reconstitution. CONCLUSION The repair genes differentially expressed after neuronal DNA damage caused by local anesthetics are mainly concentrated in the pathways of non-homologous end-joining, base excision repair and nucleotide excision repair.     

茉莉酸甲酯处理对葡萄果实NO 和H2O2 水平及植保素合成的影响

 以10 μmol · L-1 茉莉酸甲酯（Methyl jasmonate,MeJA）熏蒸处理‘巨峰’葡萄果实6 h,随后转入1 ℃下贮藏28 d。结果表明,MeJA 处理显著抑制了葡萄果实在贮藏期间腐烂率和失重率的上升,促进内源NO 释放量和H2O2 含量在贮藏前期的上升,同时诱导植保素合成相关酶苯丙氨酸解氨酶（PAL）、肉桂酸–4–羟化酶（C4H）、对香豆酰–CoA 连接酶（4-CL）和白藜芦醇合成酶（RS）活性以及植保素白藜芦醇和白藜芦醇脱氢二聚体含量的上升。由此推测,MeJA 在葡萄果实细胞内发挥了信号传导作用,通过调控下游信号分子H2O2 和NO 的水平来提高植保素合成相关酶活性,从而促进了植保素的积累,提高果实的抗病性,降低了其腐烂率。     

Effect of Mailuoning local perfusion on Wnt/β-catenin and Notch signaling pathways in crush injury syndrome model pigs

AIM To investigate the effects of local perfusion of Mailuoning on Wnt/β-catenin and Notch signaling pathway in crush injury syndrome model pigs. METHODS A total of 24 Bama mini pigs were randomly divided into normal control group， model group， normal perfusion group and Mailuoning perfusion group， with 6 in each group. Except for normal control group， the other groups were established crush injury model. After modeling， the blood supply of the pigs in model group was immediately restored. The normal perfusion group and Mailuoning perfusion group were pre-processed for modeling， and were given normal perfusion and Mailuoning perfusion for 1 h to restore their blood supply. After the recovery of blood supply for 4 h， the skeletal muscle morphology was detected by hematoxylin-eosin （HE） staining. The ultrastructure of the skeletal muscle was observed under transmission electron microscope. The serum levels of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） were measured by ELISA. The mRNA levels of vascular endothelial growth factor （VEGF） and matrix metalloproteinase-2 （MMP-2） were detected by RT-qPCR， and the protein levels of β-catenin， Delta-like ligand 4 （Dll4） and Notch in skeletal muscular tissue were observed by Western blot. RESULTS The HE results of model group showed disordered arrangement of skeletal muscle fibers， swollen or obviously constricted nucleus， shrunken sarcolemma， ruptured and swollen blood vessels， edematous interstitium， obvious infiltrating inflammatory cells. The results of electron microscopy in model group showed disorderly arranged and dissolved myofilaments， partial loss of I-band， A-line and Z-line muscle fibers， obviously swollen endoplasmic reticulum， mitochondria and nuclei， and a large number of aggregated and internally shifted nuclei. The above indexes in normal perfusion group were slightly lighter than those in model group. In Mailuoning perfusion group， the results of HE staining observation showed almost normal skeletal muscle， neatly arranged muscle fibers， almost invisible shrinkage or swelling muscle membrane， and basically returned to normal blood vessels； the results of electron microscopy showed clearly visible and regular muscle fiber I-band， A-line， Z-line and neatly arranged nuclei. Compared with normal control group， the proportion of tissue swelling and vascular damage， the percentage of abnormal Z-line， the serum levels of IL-1β and TNF-α， the mRNA expression of VEGF and MMP-2， the protein levels of nucleoprotein/total β-catenin， Dll4 and Notch in skeletal muscular tissue in model group were increased （P<0.05）. Compared with model group， the proportion of tissue swelling and vascular damage， the percentage of abnormal Z-line， the serum levels of IL-1β and TNF-α， the mRNA expression of MMP-2， the protein levels of nuclear/total β-catenin， Dll4 and Notch in skeletal muscular tissue in normal perfusion group， and the serum levels of IL-1β and TNF-α， the mRNA expression of VEGF and MMP-2， the protein levels of nuclear/total β-catenin， Dll4 and Notch in skeletal muscular tissue in Mailuoning perfusion group were decreased （P<0.05）. Compared with normal perfusion group， the proportion of tissue swelling and vascular damage， the percentage of abnormal Z-line， the serum levels of TNF-α， the mRNA expression of MMP-2， the protein levels of nuclear/total β-catenin， Dll4 and Notch in skeletal muscular tissue in Mailuoning perfusion group were decreased （P<0.05）. CONCLUSION Mailuoning local perfusion suppresses Wnt/β-catenin and Notch signaling pathways， attenuates inflammation and vascular damage， thus realizing the protection of crush injury syndrome.     

Progress in RNA-binding protein HuR and its roles in development of hepatocellular carcinoma

RNA-binding proteins （RBP） are molecules with a variety of biological functions discovered in recent years. Among them, HuR is an important RBP, widely expressed in various tissues of the body, and is a member of the Hu/embryonic lethal abnormal vision （ELAV） protein family. It mainly affects the expression levels of target genes in the cells by regulating the stability and/or translation efficiency of the mRNA of the genes, thus participating in the regulation of cell life activities. In recent years, more and more studies on HuR have revealed its important role in inflammation and cancer. This review summarizes the functions of HuR and probes into the regulation of HuR functions. In addition, the roles of HuR in the occurrence and development of hepatocellular carcinoma （HCC） are also discussed, which provides important information for exploring the pathogenesis, biomarkers and therapeutic targets of HCC.     

Effects of naringenin on PI3K/AKT signaling pathway and endoplasmic reticulum stress and its related apoptotic pathways in rats with myocardial ischemia/reperfusion injury

AIM To observe the effect of naringenin on cardiac injury in ischemia/reperfusion （I/R） rats, and to explore whether the role of naringenin is involved in PI3K/AKT signaling pathway and endoplasmic reticulum stress and its related apoptotic pathways. METHODS SD rats （n=48） were randomly divided into sham operation （sham） group, model （I/R） group, naringenin treatment （NAR） group and naringenin+LY294002 （NL） group. Myocardial I/R injury model was prepared by ligation of left anterior descending coronary artery of rats for 30 min followed by reperfusion for 120 min. After reperfusion, the serum levels of cardiac troponin I （cTnI） was measured by ELISA. HE staining, TTC staining and TUNEL staining were used to detect the myocardial histopathological changes, myocardial infarction area and myocardial cell apoptotic rate. The mRNA levels of endoplasmic reticulum stress-related indicators glucose-regulated protein 78 （GRP78）, C/EBP homologous protein （CHOP） and caspase-12 were detected by RT-qPCR. The protein levels of cleaved caspase-3, GRP78, CHOP, caspase-12, p-PI3K and p-AKT were determined by Western blot. RESULTS Compared with I/R group, the serum content of cTnI, myocardial pathological damage, myocardial infarction area and myocardial cell apoptotic rate were significantly reduced （P<0.05）, the protein levels of cleaved caspase-3, GRP78, CHOP and caspase-12 were decreased （P<0.05）, and the protein levels of p-PI3K and p-AKT were increased in NAR group （P<0.05）. LY294002 attenuated the protective effect of naringenin to some extent. CONCLUSION Naringenin reduces myocardial I/R injury in rats possibly by activating PI3K/AKT signaling pathway and subsequently regulating endoplasmic reticulum stress and its related apoptotic pathways.