苹果miR396家族鉴定及在不定根发育过程中的表达分析

分析了苹果miR396家族进化特性及其在苹果不定根发育过程中的表达模式。结果表明:苹果miR396家族有4条成熟体和7条前体序列(pre-miRNA)。Mfold预测显示Pre-miR396家族7个成员序列均可形成典型稳定的茎环二级结构,最小折叠自由能介于–62.9 kal·mol~(-1)(pre-miR396b)～–51.9kal·mol~(-1)(pre-miR396g)之间。系统发育进化树分析显示,pre-miR396家族亲缘关系可分为3个亚组(G1、G2、G3),每个亚组内基因数量不同,分别含有11、9、19个。靶基因预测显示,苹果miR396靶基因包括MdGRF1、MdGRF2和MdGRF5等,降解组测序进一步验证了mi R396对其候选靶基因MdGRF1、MdGRF2和MdGRF5的剪切关系。苹果miR396家族成员在侧根和果实中的表达量显著高于其他组织,其候选靶基因表达量则在花芽和腋芽中显著高于其他组织;不定根发育过程中,miR396家族不同成员表达模式存在显著差异,整体上呈上调表达趋势,其候选靶基因呈下调表达趋势;外源IBA处理显著诱导miR396家族成员的表达,尤其是在不定根诱导期和根系生长期更为显著。     

龙眼miR166家族的分子进化特性及时空表达分析

为了解miR166基因家族的分子进化特性及其在龙眼不同组织部位的表达规律,对龙眼miR166家族成员的成熟体和前体序列及其进化、前体二级结构预测、靶基因预测以及时空表达模式进行了分析。结果表明:龙眼miR166家族含有12条成熟体序列和7个前体序列(pre-miRNA)。Mfold预测显示pre-miR166家族7个成员的序列均能形成典型稳定的茎环二级结构,成熟序列的碱基保守性高,其他位置的则保守性减弱;它们的最小折叠自由能(ΔG)在–35.30~–83.30kal·mol~(-1)。系统发育进化树分析显示,龙眼pre-miR166家族与葡萄、碧桃的pre-miR166亲缘关系更为接近。靶基因预测显示,龙眼miR166基因家族靶基因包括同源异型域—亮氨酸拉链蛋白、三角状五肽重复结构蛋白、假定蛋白、DNA指导的RNA聚合酶Ⅲ亚单位RPC2、紫外线B受体等。实时荧光定量PCR显示,pre-miR166家族不同成员在龙眼生长发育进程中均有表达且表达模式不尽相同,提示其可能广泛参与龙眼各个器官的调控,且在功能上可能具有分工。     

miR395分子进化特性及其在龙眼早期体胚发生中的表达分析

【目的】研究miR395的分子进化特性及其在龙眼早期体胚发生中的表达分析。【方法】通过龙眼miRNA文库、转录组数据库和miRBase数据库,得到所有植物miR395家族成员成熟体和前体序列,对其进行序列比对及进化分析、保守性分析、前体二级结构预测、潜在靶基因预测,对龙眼miR395a在龙眼早期体胚发生(SE)阶段的表达模式进行分析。【结果】龙眼miR395家族包含5条前体序列和2条成熟体序列。Mfold预测分析发现,龙眼pre-miR395序列均能形成稳定的发卡结构,其最小折叠自由能ΔG在-44.70～64.80 kal·mol-1,提示与序列长度没有显著相关性。其次,保守性分析显示,植物pre-miR395两端序列较保守,而中间序列不保守;系统进化分析提示,龙眼pre-miR395家族与脐橙、葡萄和苹果的亲缘关系更近。psRNAtarget预测显示,龙眼miR395调控的潜在靶基因主要包含富含亮氨酸重复受体蛋白激酶LRR-RLKs、ATP硫酸化酶APS1、蛋白磷酸酶PP2C、前体RNA蛋白质TSR1同系物TSR1、酮酯酰CoA硫解酶KAT2和EH结构域蛋白EHD1等6个,且都是以裂解靶标的方式进行调控。qRT-PCR分析表明,在龙眼早期体胚发生阶段,miR395a呈上调趋势,且miR395a与APS1呈显著负相关。【结论】龙眼miR395与其他植物miR395功能具有高度保守性和物种特异性,同时龙眼miR395a上调表达可能促进龙眼球形胚的形态建成。     

龙眼miR172家族成员进化特性及其时空表达分析

【目的】研究龙眼miR172家族的进化特性及其在龙眼不同组织部位中的表达模式。【方法】采用生物信息学分析及实时荧光定量PCR的方法,对龙眼miR172家族5条前体(pre-miR172)序列及1条成熟体序列进行分析,并预测其前体二级结构,构建系统发育进化树,预测靶基因及分析不同组织部位的定量表达情况。【结果】对龙眼miR172家族5条前体序列进行多序列比对,发现miR172家族两端相对保守,中间区域则形成各自的特异性区域。对miR172家族5条前体及1条成熟体进行多序列比对,发现6条序列间存在1个约20个碱基的保守区域,推测该区域可能为miR172家族成熟体所在区域。Mfold软件预测结果显示,pre-miR172家族成员均能形成典型的茎环二级结构,其最小折叠自由能为-35.80~-54.45 kal·mol-1,较为稳定。系统发育进化树结果显示,龙眼pre-miR172家族成员与甜橙、毛果杨等植物的miR172亲缘关系较近。靶基因预测结果显示,龙眼miR172a的靶基因包括AP2、蝶呤型钼辅因子(molybdopterin cofactor)、谷氨酰-t RNA(glutamyl-t RNA)、假定蛋白(hypothetical protein)等。实时荧光定量PCR结果显示,miR172家族各成员在龙眼不同组织部位中的表达模式总体相似,均在叶芽和生殖生长阶段中大量表达,在营养生长阶段及果实中表达量则较低,但dlo-miR172-scaffold4293特异地在叶片中高表达。【结论】龙眼miR172家族在进化过程中保守性与特异性并存,且可能参与了龙眼部分器官的形成及发育过程。     

miR168家族进化特性及其在砂梨休眠期的表达模式分析

为了探究miR168家族的进化特性及其在梨休眠进程中的表达模式,通过检索实验室前期构建的砂梨（‘黄花’梨）miRNA文库、转录组数据库和miRBase数据库,得到植物miR168家族成员的成熟体和前体序列。从‘黄花’梨花芽中克隆了两条miR168前体,发现梨miR168家族包含2条前体序列和4条成熟体序列。采用生物信息分析和实时荧光定量PCR(qRT-PCR),对梨miR168家族的成熟体序列及前体（pre-miR168）序列进行分析,与已知植物miR168构建系统发育进化树,预测其靶基因,分析其在梨休眠发生进程中的表达情况。结果表明,梨pre-miR168序列均能形成稳定的发夹结构;植物pre-miR168两端序列较保守,而中间序列不保守;mi168成熟体保守性较高,进化树分析表明梨pre-miR168与苹果的亲缘关系最近,miR168成熟体主要分为两大类。梨miR168调控的潜在靶基因主要包含Argonaute1蛋白基因（protein argonaute 1,AGO1）和胼胝质合成酶3基因（callose synthase 3,CalS3）共21条mRNA,都是以裂解靶标的方式进...     

‘库尔勒香梨’miR159家族成员进化特性及表达分析

【目的】了解‘库尔勒香梨’miR159家族成员的进化特征及其在萼片脱落与宿存中的作用。【方法】以‘库尔勒香梨’Small RNA高通量测序中获得的miR159家族前体序列和成熟体序列为基础进行系统发育树构建、前体和成熟体的序列比对、前体二级结构预测、WebLogo保守性分析、靶基因预测和表达量分析。【结果】‘库尔勒香梨’miR159家族存在2个前体成员(psi-MIR159a、psi-MIR159c)和2个成熟体成员(psi-miR159a、psi-miR159c)。2个前体成员的序列均能形成典型稳定的茎环结构,且序列完全一致,它们的最小折叠自由能(dG)都为-93.95 kal·mol~(-1)。系统发育进化树显示,‘库尔勒香梨’和苹果MIR159家族亲缘关系很近。WebLogo分析表明,miR159家族成熟体的保守性很高,其保守序列为5'-UUUGGAUUGAAGGGAGCUCUAUU-3',但‘库尔勒香梨’的碱基保守性较低。靶基因预测显示,‘库尔勒香梨’miR159基因家族靶基因为转录因子bHLH91、BES1/BZR1同源蛋白4、热激70 ku蛋白质、Trihelix转录因子GT-1、G型凝集素S-受体类丝氨酸/苏氨酸蛋白激酶RLK1等。实时荧光定量PCR(qPCR)显示,‘库尔勒香梨’miR159家族的2个成员在初花期、盛花期和末花期3个时期萼片脱落组和宿存组的表达量有显著差异。【结论】‘库尔勒香梨’miR159家族在进化过程中既有保守性又有多样性,可能在萼片脱落过程中起作用。     

苹果全基因组CRF家族成员鉴定及在不定根发育过程中的表达分析

通过生物信息学分析,从‘金冠’苹果基因组鉴定得到了11个细胞分裂素响应因子（CRF）基因。根据基因在染色体上的位置,将其依次命名为MdCRF1 ~ MdCRF11,并对其进行理化特性、基因结构、系统进化和启动子元件分析。MdCRF编码的蛋白在137 ~ 435 aa之间,等电点在4.26 ~ 9.68之间。基因结构分析发现,MdCRF1有2个外显子1个内含子,MdCRF11有3个外显子2个内含子,其余基因都只含有外显子,没有内含子;保守基序列分析发现,MdCRF蛋白的保守基序数量在5 ~ 9。通过系统进化分析将家族成员分为G1、G2和G3共3个亚组,每个亚组内成员数量相对均匀。组织特异性表达分析发现11个基因在不同杂交种苹果和不同器官中的表达量存在明显差异。以苹果砧木‘T337’为材料,qPCR验证了MdCRF家族基因大部分在根、茎、愈伤组织中高表达,同时也响应生根处理表达量发生显著下调。对11个MdCRF蛋白之间的网络调控关系进行了研究,分析预测了相关基因间的潜在联系。结合分析可知,其中MdCRF8、MdCRF10和MdCRF11可能参与调控苹果砧木不定根发育。     

苹果CR4基因家族鉴定与表达分析

以RCC1（PF00415）、TNFR_c6（PF00020）和Pkinase（PF00069）保守域全蛋白序列为种子序列,在苹果全基因组范围比对分析了CRINKLY4（CR4）家族成员,对其理化性质、进化关系、染色体分布等进行了分析;基于qPCR分析了CR4基因在苹果腐烂病发生和低温胁迫过程中的表达情况。通过分析,共获得8个苹果CR4基因,其氨基酸序列大小介于668 ~ 1 690,分子量介于71.73 ~ 187.61 kD,等电点介于5.69 ~ 8.66,主要位于质膜;根据进化分析将其分为两个亚组。PCR表达分析结果表明,CR4基因在苹果不同组织和品种间存在不同的表达模式。分别有8个和6个CR4基因在苹果花芽感受低温和接种腐烂病菌后至少在1个时间点发生差异表达。其中,MD03G1068800在花芽感受低温后上调达25倍以上,而MD00G1166500和MD01G1153100在腐烂病发生后上调达150倍以上,以上3个CR4基因可作为后续功能研究的候选基因。     

苹果LysM类受体激酶基因家族鉴定与表达分析

以LysM(PF01476)和Pkinase(PF00069)保守域全蛋白序列为种子序列,在全基因组范围比对分析了苹果(Malus×domestica Borkh.)LysM-RLK家族的成员,对其家族成员的理化性质、进化关系、染色体分布、基因结构等进行了分析;基于已公布的转录组学数据,分析了LysM-RLK基因在苹果组织、发育过程和生物胁迫中的表达情况。通过分析,共获得12个苹果LysM-RLK基因,其氨基酸序列大小介于553~1 053,分子量介于62.65~119.04 kD,等电点介于5.11~7.45,主要位于质膜;根据进化分析将其分为3个亚组,亚组内各成员的外显子—内含子结构呈现较为相似的特征。基因表达数据显示,苹果的4个LysM-RLK基因表达存在较大的组织特异性,7个基因在苹果腐烂病和再植病发病过程中为差异表达。     

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.     

Prostaglandin E1 protects heart after myocardial infarction by inhibiting endoplasmic reticulum stress in rats

AIM To investigate the effect of prostaglandin E1 (PGE1) on heart after myocardial infarction (MI) in rats and its related molecular mechanism. METHODS Fifty male SD rats were divided into sham group, model group and model+PGE1 group. The MI rat model was established by ligation of left anterior descending coronary artery. Cardiac function in the rats was detected by echocardiogaphy. The myocardial histomorphologic changes were evaluated by HE and Masson staining. The MI area was measured by TTC staining. The cardiomyocyte death was detected by TUNEL staining. The protein levels of endoplasmic reticulum stress (ERS)-related factors glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12, and apoptosis-related factors Bcl-2, Bax and cleaved caspase-3 were determined by immunofluorescence staining and Western blot. RESULTS Compared with sham group, the cardiac function in model group was decreased, with significant myocardial pathological changes. The MI area was enlarged, and the death of cardiomyocytes was promoted. The protein levels of GRP78, CHOP, caspase-12, Bax and cleaved caspase-3 in the myocardial tissues were significantly increased, while Bcl-2 was decreased (P<0.01). Compared with model group, the cardiac function in model+PGE1 group was significantly improved, and the myocardial pathological damage was significantlty attenuated. The MI area and myocardial cell death were significantly reduced. The protein levels of GRP78, CHOP, caspase-12, Bax and cleaved caspase-3 in the myocardial tissues were significantly decreased, while Bcl-2 was increased (P<0.01). CONCLUSION PGE1 reduces collagen deposition and inflammation, and improves cardiac function by reducing ERS level, thus protecting cardiomyocytes from MI damage.     

Effect of Jinlida combined with Tongxinluo on apoptosis of renal microvascular endothelial cells in high-glucose environment

AIM To observe the effect of Jinlida combined with Tongxinluo on the apoptosis of renal microvascular endothelial cells in the high-glucose environment, and to explore their mechanism of protecting renal microvascular endothelial cells. METHODS The renal microvascular endothelial cells cultured in vitro were divided into control group, high glucose group, Tongxinluo group, Jinlida group, and Tongxinluo+Jinlida group. After intervention for 24 h, CCK-8 assay was used to measurethe cell viability. The apoptotic rate and reactive oxygen species (ROS) level were measured by flow cytometry. Western blot was used to determine the protein levels of protein kinase R-like endoplasmic reticulum kinase (PERK), phosphorylated PERK (p-PERK), glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), caspase-12 and Bcl-2. RESULTS Compared with control group, the viability of renal microvascular endothelial cells in the high-glucose environment was decreased, the apoptotic rate, the ROS level and the protein levels of PERK, p-PERK, GRP78, CHOP and caspase-12 were increased, while Bcl-2 protein was decreased (P<0.05). In comparison with high glucose group, the viability of renal microvascular endothelial cells in Tongxinluo, Jinlida and Tongxinluo+Jinlida groups was increased to varying degrees, the apoptotic rate, the ROS level and the protein levels of PERK, p-PERK, GRP78, CHOP and caspase-12 were decreased, while Bcl-2 protein was increased (P<0.05). Compared with Jinlida group and Tongxinluo group, the improvement of each index in Jinlida+Tongxinluo group was statistically significant. CONCLUSION Jinlida and Tongxinluo attenuate the damage of renal microvascular endothelial cells in the high-glucose environment, and the mechanism may be related to the reduction of endoplasmic reticulum stress-mediated apoptosis pathway. The combined application of Jinlida and Tongxinluo synergistically enhances the protective effect of the drugs on the renal microvascular endothelial cells.     

Autophagy induces mitochondrial dysfunction in neurons from neonatal rats with hypoxic ischemic encephalopathy

AIM: To explore the influence of autophagy on the induction of mitochondrial dysfunction in the neurons in a neonatal rat hypoxic ischemic encephalopathy (HIE) model. METHODS: Ten-day-old rat pups (n=30) were randomly divided into sham group and model group. The rats in the latter group were subject to hypoxia-ischemia treatment via unilateral common carotid artery ligation. The rats were sacrificed for brain pathological examination, and the protein levels of cleaved caspase-3 and LC3B-II were detected by immunohistochemical analysis. For the in vitro experiments, the autophagy of primarily cultured rat neurons was observed after hypoxia, and Western blot and mitochondrial function testing were also performed. RESULTS: Compare with sham group, the hypoxia-ischemia treatment caused atrophy and apoptosis of neurons, and ventricular area enlargement of rat brains. Immunohistochemical results demonstrated significantly higher levels of apoptosis- and autophagy-associated proteins, such as cleaved caspase-3 and LC3B-II (P<0.01). In vitro experiments demonstrated that hypoxia induced autophagy and apoptosis in the neurons. Compared with sham group, there were higher levels of reactive oxygen species and mitochondrial superoxide, and lower mitochondrial membrane potential in the model group (P<0.01). CONCLUSION: In neonatal HIE rat model, the hypoxia-induced mitochondrial dysfunction is related to apoptosis and autophagy. It will provide a new idea for administration of autopahgy inducer agents in treatment of HIE.     

Relationship between histone H3K36 trimethylation and acute renal injury induced by ischemia/reperfusion

AIM: To observe the expression change of H3K36 trimethylation (H3K36me3) in acute kidney injury (AKI) induced by ischemia/reperfusion (IR) and analyze its correlation with SMYD2 and renal injury, and to provide a new target for clinical treatment of IR-AKI. METHODS: The ICR mice (n=30) were randomly divided into IR group (n=15) and sham operation group (sham group, n=15). The AKI model was established by clamping bilateral renal pedicles for 45 min. The serum and renal tissues of the mice were collected after the model was established for 24 h. The levels of blood urea nitrogen (BUN) and serum creatinine (SCr) were detected by biochemical method. The pathological changes of the kidney were observed by HE staining. The changes of NGAL and cleaved caspase-3 were observed by immunohistochemical (IHC) staining. The protein levels of NGAL, SMYD2, H3K36me3, p-P53, P53, cleaved caspase-3, Bax, Bcl-2, STAT3, p-STAT3, JNK and p-JNK1/2/3 in the renal tissues were determined by Western blot. The relationship between H3K36me3 and SMYD2/NGAL was analyzed by Pearson correlation method. RESULTS: Compared with sham group, BUN and SCr levels of the mice in IR group were significantly increased (P<0.05). HE staining showed significant edema, abscission and necrosis in renal tubular epithelial cells of the micc in IR group, and abscission of brush border and large amount of cell debris in the lumen were also observed. The IHC staining results showed that the protein levels of NGAL and cleaved caspase-3 in IR group were significantly increased. The results of Western blot showed that the protein levels of NGAL, SMYD2, H3K36me3, p-P53, cleaved caspase-3, Bax, STAT3, p-STAT3, JNK and p-JNK1/2/3 in IR group were significantly up-regulated (P<0.05), while the Bcl-2 levels were significantly down-regulated (P<0.05). The correlation analysis showed that H3K36me3 was positively correlated with the levels of SMYD2 and NGAL. CONCLUSION: H3K36me3 is closely related to SMYD2 and renal injury in IR-AKI mice, and the up-regulated expression of H3K36me3 may be involved in the regulation of IR-AKI occurrence and development together with the activation of STAT3 and JNK signaling pathways.     

IL-33-modified BMSCs attenuate acute kidney injury induced by sepsis in rats through MyD88

AIM To investigate the effect of interleukin-33 (IL-33)-modified bone marrow mesenchymal stem cells (BMSCs) on sepsis-induced acute kidney injury (AKI) in rats and the expression of myeloid differentiation factor 88(MyD88). METHODS A septic rat model was established by cecal ligation and puncture. The SD rats (n=80) were randomly divided into control group, model group, negative transfection group (transplanting untransfected BMSCs) and IL-33 transfection group (transplanting BMSCs transfected with IL-33), with 20 in each group. Survival rates of the rats within 72 h in the 4 groups were compared. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were measured before, and 24, 48 and 72 h after transplantation. The kidney pathological damage was observed by HE staining, and the apoptosis of renal cells was detected by TUNEL method 72 h after transplantation. Western blot was used to detect the protein expression levels of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), Toll-like receptor 4 (TLR4) and MyD88. RESULTS The survival rate of the rats in model group was significantly lower than that in control group (P<0.05). The survival rate of the rats in IL-33 transfection group was higher than that in model group and negative transfection group (P<0.05). The levels of SCr and BUN in model group were higher than those in control group (P<0.05). The levels of SCr and BUN in IL-33 transfection group were significantly reduced after transplantation, and were lower than those in model group and negative transfection group (P<0.05). The renal tissue pathological injury score in model group was significantly higher than that in control group (P<0.05). Compared with model group and negative transfection group, the renal tissue pathological injury score in IL-33 transfection group was significantly reduced (P<0.05). The proportion of apoptotic cells in the kidney tissues in model group were higher than that in control group (P<0.05). Compared with model group and negative transfection group, the proportion of apoptotic cells in the kidney tissues in IL-33 transfection group was significantly reduced (P<0.05). The protein expression levels of IL-1β, IL-6, TNF-α, TLR4 and MyD88 in model group were significantly higher than those in control group (P<0.05). Compared with model group and negative transfection group, the protein expression levels of IL-1β, IL-6, TNF-α, TLR4 and MyD88 in IL-33 transfection group were significantly decreased (P<0.05). CONCLUSION IL-33 gene-modified BMSCs significantly improve the renal function of AKI rats with sepsis. The mechanism may be related to IL-33 regulating TLR4/MyD88 signaling pathway and inhibiting renal inflammatory response.     

Protective effect of morinda officinalis oligosaccharides monomer HexB on hypoxia/reoxygenation-induced injury in HUVECs

AIM:To explore the protective effect of morinda officinalis oligosaccharides monomer HexB on hypoxia/reoxygenation (H/R)-induced injury in human umbilical vein endothelia cells (HUVECs). METHODS:HUVECs were treated with HexB, 4-phenylbutyric acid (4-PBA) and thapsigargin (TG), respectively. The cells were divided into control group, HexB group, H/R group, HexB+H/R group, 4-PBA+H/R group, TG group and HexB+TG group. The cell viability was measured by CCK-8 assay. The apoptotic rate was detected by flow cytometry. Western blot was used to determine the protein levels of endoplasmic reticulum stress (ERS) related molecules chaperone protein glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), apoptosis-related protein caspase-12 and phosphorylated c-Jun NH₂-terminal kinase (p-JNK). RESULTS:The viability of HUVECs was reduced in H/R group and TG group (P<0.05), increased in HexB+H/R, 4-PBA+H/R and HexB+TG group (P<0.05). The apoptotic rate, the protein levels of GRP78, CHOP, caspase-12 and p-JNK were increased in H/R group and TG group (P<0.05), weakened in the HexB+H/R group (P<0.05), 4-PBA+H/R group and HexB+TG group (P<0.05). No significant change in the apoptotic rate, cell viability, protein levels of GRP78, CHOP, caspase-12, p-JNK between HexB+H/R group and 4-PBA+H/R group was observed. CONCLUSION:HexB attenuates HUVECs injury caused by H/R through suppressing ERS and apoptosis. The possible mechanism may be involved in the apoptotic pathways related to GRP78, CHOP, caspase-12 and p-JNK.