Structure,Binding Characteristics,and 3D Model Prediction of a Newly Identified Odorant-Binding Protein from the Cotton Bollworm,Helicoverpa armigera (Hübner)

The full-length sequence of the odorant binding protein 5 gene,HarmOBP5,was obtained from an antennae cDNA library of cotton bollworm,Helicoverpa armigera （Hübner）.The cDNA contains a 444 bp open reading frame,encoding a protein with 147 amino acids,namely HarmOBP5.HarmOBP5 was expressed in Escherichia coli and the recombinant protein was purified by affinity chromatography.SDS-PAGE and Western blot analysis demonstrated that the purified protein can be used for further investigation of its binding characteristics.Competitive binding assays with 113 odorant chemicals indicated that HarmOBP5 has strong affinity to some special plant volatiles,including （E）-β-farnesene,ethyl butyrate,ethyl heptanoate,and acetic acid 2-methylbutyl ester.Based on three-dimensional （3D） model of AaegOBP1 from Aedes aegypti,a 3D model of HarmOBP5 was predicted.The model revealed that some key binding residues in HarmOBP5 may play important roles in odorant perception of H.armigera.This study provides clues for better understanding physiological functions of OBPs in H.armigera and other insects.

Histone H3K27me3 methylation regulates the expression of secreted proteins distributed at fast-evolving regions through transcriptional repression of transposable elements

The fine-tuned expression dynamics of the effector genes are pivotal for the transition from vegetative growth to host colonization of pathogenic filamentous fungi.However,mechanisms underlying the dynamic regulation of these genes remain largely unknown.Here,through comparative transcriptome and chromatin immunoprecipitation sequencing(ChIP-seq)analyses of the methyltransferase PoKmt6 in rice blast fungus Pyricularia oryzae(syn.Magnaporthe oryzae),we found that PoKmt6-mediated H3K27me3 deposition was enriched mainly at fast-evolving regions and contributed to the silencing of a subset of secreted proteins(SP)and transposable element(TE)families during the vegetative growth of P.oryzae.Intriguingly,we observed that a group of SP genes,which were depleted of H3K27me3 modification,could also be silenced via the H3K27me3-mediated repression of the nearby TEs.In conclusion,our results indicate that H3K27me3 modification mediated by PoKmt6 regulates the expression of some SP genes in fast-evolving regions through the suppression of nearby TEs.

NF-E2:a Novel Regulator of Alpha-hemoglobin Stabilizing Protein Gene Expression

Objective To investigate whether α-hemoglobin stabilizing protein (AHSP), the α-globin-specific molecular chaperone, is regulated by erythroid transcription factor NF-E2. Methods We established the stable cell line with NF-E2p45 (the larger subunit of NF-E2) short hairpin RNA to silence its expression. Western blot, real-time polymerase chain reaction, and chromatin immunoprecipitation (ChIP) analysis were performed to detect the expression of AHSP, the histone modifications at AHSP gene locus, and the binding of GATA-1 at the AHSP promoter with NF-E2p45 deficiency. ChIP was also carried out in dimethyl sulfoxide (DMSO)-induced DS19 cells and estrogen-induced G1E-ER4 cells to examine NF-E2 binding to the AHSP gene locus and its changes during cell erythroid differentiation. Finally, luciferase assay was applied in HeLa cells transfected with AHSP promoter fragments to examine AHSP promoter activity in the presence of exogenous NF-E2p45. Results We found that AHSP expression was highly dependent on NF-E2p45. NF-E2 bound to the regions across AHSP gene locus in vivo, and the transcription of AHSP was transactivated by exogenous NF-E2p45. In addition, we observed the decrease of H3K4 trimethylation and GATA-1 occupancy at the AHSP gene locus in NF-E2p45-deficient cells. Restoration of GATA-1 in G1E-ER4 cells in turn led to increased DNA binding of NF-E2p45. Conclusion NF-E2 may play an important role in AHSP gene regulation, providing new insights into the molecular mechanisms underlying the erythroid-specific expression of AHSP as well as new possibilities for β-thalassemia treatment.

Epigenetic Repression of SATB1 by Polycomb Group Protein EZH2 in Epithelial Cells

Objective To study the regulatory mechanism of SATB1 repression in cells other than T cells or erythroid cells, which have high expression level of SATB1. Methods HeLa epithelial cells were treated with either histone deacetylase inhibitor (HDACi) trichostatin A (TSA) or DNA methylation inhibitor 5-Aza-C before detecting SATB1 expression. Luciferase reporter system was applied to measure effects of EZH2 on SATB1 promoter activity. Over-expression or knockdown of EZH2 and subsequent quantitative reverse transcription-polymerase chain reaction were performed to determine the effect of this Polycomb group protein on SATB1 transcription. Chromatin immunoprecipitation (ChIP) assay was applied to measure enrichment of EZH2 and trimethylated H3K27 (H3K27me3) at SATB1 promoter in HeLa cells. K562 cells and Jurkat cells, both having high-level expression of SATB1, were used in the ChIP experiment as controls. Results Both TSA and 5-Aza-C increased SATB1 expression in HeLa cells. Over-expression of EZH2 reduced promoter activity as well as the mRNA level of SATB1, while knockdown of EZH2 apparently enhanced SATB1 expression in HeLa cells but not in K562 cells and Jurkat cells. ChIP assay results suggested that epigenetic silencing of SATB1 by EZH2 in HeLa cells was mediated by trimethylation modification of H3K27. In contrast, enrichment of EZH2 and H3K27me3 was not detected within proximal promoter region of SATB1 in either K562 or Jurkat cells. Conclusion SATB1 is a bona fide EZH2 target gene in HeLa cells and the repression of SATB1 by EZH2 may be mediated by trimethylation modification on H3K27.

Loss of LBP triggers lipid metabolic disorder through H3K27 acetylation-mediated C/EBPβ-SCD activation in non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease(NAFLD)is associated with mutations in lipopolysaccharide-binding protein(LBP),but the underlying epigenetic mechanisms remain understudied.Herein,LBP^(-/-)rats with NAFLD were established and used to conduct integrative targetingactive enhancer histone H3 lysine 27 acetylation(H3K27ac)chromatin immunoprecipitation coupled with high-throughput and transcriptomic sequencing analysis to explore the potential epigenetic pathomechanisms of active enhancers of NAFLD exacerbation upon LBP deficiency.Notably,LBP^(-/-)reduced the inflammatory response but markedly aggravated high-fat diet(HFD)-induced NAFLD in rats,with pronounced alterations in the histone acetylome and regulatory transcriptome.In total,1128 differential enhancer-target genes significantly enriched in cholesterol and fatty acid metabolism were identified between wild-type(WT)and LBP^(-/-)NAFLD rats.Based on integrative analysis,CCAAT/enhancer-binding proteinβ(C/EBPβ)was identified as a pivotal transcription factor(TF)and contributor to dysregulated histone acetylome H3K27ac,and the lipid metabolism gene SCD was identified as a downstream effector exacerbating NAFLD.This study not only broadens our understanding of the essential role of LBP in the pathogenesis of NAFLD from an epigenetics perspective but also identifies key TF C/EBPβand functional gene SCD as potential regulators and therapeutic targets.

Arabidopsis PWWP domain proteins mediate H_3K_(27) trimethylation on FLC and regulate flowering time

LHP1 mediates recruitment of the PRC2 histone methyltransferase complex to chromatin and thereby facilitates maintenance of H3K27me3 on FLC, a key flowering repressor gene. Here, we report that the PWWP domain proteins （PDPs） interact with FVE and MSI5 to suppress FLC expression and thereby promote flowering. We demonstrated that FVE, MSI5, and PDP3 were co-purified with LHP1. The H3K27me3 level on FLC was decreased in the pdp mutants as welt as in the fve/ msi5 double mutant. This study suggests that PDPs function together with FVE and MSI5 to regulate the function of the PRC2 complex on FLC.

Emergence of truncated PB1-F2 protein of H3N2 influenza virus during its epidemic period in Jiangsu Province, China

Background PB1-F2 protein has been proven to increase the pathogenicity of influenza A virus （IAV） strains in primary infection and in secondary bacterial infection. It can also regulate the activity of viral polymerase. However, it was shown in another retrospective study that a portion of IAVs do not express full-length PB1-F2 protein during virus development; different kinds of stop codons cause exits in the open reading frames and form PB1-F2 gene products with the corresponding genotypes. Truncated PB1-F2 in human H3N2 IAVs has long been detected in North America but its evolution in China is still unclear. Methods Influenza-like illnesses （ILls） from the whole of Jiangsu Province were collected and inspected to determine the type and subtype of the viruses. A portion of isolates collected in the epidemic period were selected as samples for later whole-genome sequencing, and the exact sequences were determined and analyzed. Results H3N2 influenza virus was one of the epidemical strains which had been prevalent during 2009-2010, in Jiangsu. Five H3N2 isolates with truncated PB1-F2 protein （25aa） were detected in influenza samples from Nanjing and Xuzhou, while seven similar H3N2 isolates were also reported in Niigata, Japan. Conclusion This emergence indicates the possibility that there has been transmission of the H3N2 virus between the two countries.

绝经后H型高血压合并骨质疏松症患者血清MCP-1、PTX3、GDF15的变化及其临床意义分析

目的分析绝经后H型高血压(HHT)合并骨质疏松症(OP)患者血清单核细胞趋化蛋白(MCP)-1、正五聚蛋白3(PTX3)、生长分化因子15(GDF15)的变化及其临床意义。方法选取2020年6月至2023年5月我院收治的127例绝经后HHT合并OP患者为研究组,另选取同期85例绝经后OP患者为OP组,62例绝经后单纯HHT患者为HHT组、60例体检健康的绝经后女性志愿者为健康组。比较4组血清MCP-1、PTX3、GDF15水平、股骨颈和腰椎(L_(1~4))骨密度、血清骨代谢指标[骨钙素(BGP)、Ⅰ型胶原羧基端肽β特殊序列(β-CTX)、Ⅰ型前胶原氨基端前肽(PINP)]及炎症因子[肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)]。采用Pearson相关性分析血清MCP-1、PTX3、GDF15水平与骨密度、血清骨代谢指标及炎症因子的相关性。采用受试者工作特征(ROC)曲线分析血清MCP-1、PTX3、GDF15对绝经后HHT合并OP的诊断价值。结果与健康组比较,OP组、HHT组及研究组血清MCP-1、PTX3、GDF15、BGP、β-CTX、PINP水平均较高,且OP组高于HHT组,研究组高于OP组和HHT组(P<0.05)。与健康组比较,OP组、HHT组及研究组血清TNF-α、IL-6水平均较高,且HHT组高于OP组,研究组高于OP组和HHT组(P<0.05)。与健康组比较,OP组、HHT组及研究组的股骨颈和腰椎(L_(1~4))骨密度均较低,且OP组低于HHT组,研究组低于OP组和HHT组(P<0.05)。Pearson相关性分析显示,血清MCP-1、PTX3、GDF15水平与股骨颈和腰椎(L_(1~4))骨密度呈负相关,与血清BGP、β-CTX、PINP、TNF-α、IL-6水平呈正相关(P<0.05)。ROC曲线分析显示,血清MCP-1、PTX3、GDF15联合诊断绝经后HHT合并OP的AUC值为0.945,高于单独指标诊断。结论绝经后HHT合并OP患者血清MCP-1、PTX3、GDF15水平升高,且与股骨颈和腰椎(L_(1~4))骨密度、血清骨代谢指标及炎症因子密切相关,三者联合检测对诊断绝经后HHT合并OP患者有较高价值。

JASMONATE-ZIM DOMAIN proteins engage Polycomb chromatin modifiers to modulate Jasmonate signaling in Arabidopsis

Jasmonate(JA)regulates various aspects of plant growth and development and stress responses,with prominent roles in male reproductive development and defenses against herbivores and necrotrophic pathogens.JASMONATE-ZIM DOMAIN(JAZ)proteins are key regulators in the JA signaling pathway and function to repress the expression of JA-responsive genes.Here,we show that JAZ proteins directly interact with several chromatin-associated Polycomb proteins to mediate repressive chromatin modifications at JA-responsive genes and,thus,their transcriptional repression in Arabidopsis.Genetic analyses revealed that the developmental defects,including anther and pollen abnormalities,resulting from loss or block of JA signaling were partially rescued by loss of Polycomb protein-mediated chromatin silencing(Polycomb repression).We further found that JAZ-mediated transcriptional repression during anther and pollen development requires Polycomb proteins at four key Regulatory loci.Analysis of genome-wide occupancy of a Polycomb factor and transcriptome reprogramming in response to JA revealed that Polycomb repression is involved in the repression of various JA-responsive genes.Taken together,our study reveals an important chromatin-based mechanism for JAZ-mediated transcriptional repression and JA signaling in plants.

低蛋白日粮对生长猪舍NH_3和H_2S质量浓度及猪生产性能的影响

将 48头平均体重约 2 7kg的杜× (长×大 )三元杂交生长猪根据体重和性别分成 4组 ,饲喂 4种不同蛋白质水平日粮 ,3种试验日粮根据理想氨基酸模式配制。试验结果表明 :① 4组日增重与料重比差异不显著 (P >0 .0 5 )。 15 %粗蛋白组生长速度最快 ,14 %粗蛋白组经济性能最好 ,平均增重利润比 17%粗蛋白组多 0 .41元 /kg。② 14 %、13 %粗蛋白组血清尿素氮分别显著 (P <0 .0 5 )、极显著 (P <0 .0 1)低于 17%粗蛋白组。③ 4组猪舍期中、期末氨气质量浓度 ,14 %、13 %粗蛋白组分别显著 (P <0 .0 5 )、极显著 (P <0 .0 1)低于 17%粗蛋白组 ,各组硫化氢质量浓度无显著差异 (P >0 .0 5 )。

组胺H_3受体对垂体瘤AtT-20细胞分泌ACTH的调节作用

目的 观察组胺受体激动剂对 At T- 2 0细胞分泌ACTH的影响 ,并探讨 G蛋白在组胺 H3受体信号转导机制中的作用 .方法 选用文献报道的高表达组胺 H3受体的垂体细胞瘤 At T- 2 0作为观察系统 ,用放免分析法测定给予组胺受体激动剂后各时间点细胞上清液中 ACTH分泌量的变化 ,并观察药物对细胞增殖的影响 .结果 组胺 H3受体激动剂R- (α) - Me HA(0 .1μmol· L- 1 )作用 8h能明显促进 ACTH的释放 ,释放量为 192 0 μg· L- 1 ,与同时间对照组 (780 μg·L- 1 )相比 ,明显增高 (P<0 .0 1) ;H1 和 H2 激动剂则无此作用 .且 R- (α) - Me HA引起 ACTH分泌的效应能被 H3受体特异性拮抗剂 thioperamide所拮抗 ,而 H1 受体和 H2 受体拮抗剂均不影响 R- (α) - Me HA的效应 .R- (α) - Me HA作用 8和 2 4h,对细胞增殖无明显影响 .用 G蛋白失活剂 NEM预先处理细胞后 ,取消了 R- (α) - Me HA增强 At T- 2 0细胞 ACTH分泌的效应 .结论 特异性激动组胺 H3受体后能引起兴奋 -分泌耦联过程 ,其信号转导过程中有 G蛋白的参与 .

Association of CFH and MAP1LC3B gene polymorphisms with age-related macular degeneration in a high-altitude population

AIM: To evaluate the association of complement factor H(CFH) and microtubule-associated protein 1 light chain 3 beta(MAP1LC3B) gene polymorphisms with the risk of age-related macular degeneration(AMD) in a high-altitude population. METHODS: The study group consisted of 172 participants with symptoms of AMD who were examined and diagnosed between January 2019 and June 2020. The control group was composed of 120 healthy individuals. Each participant was required to provide two milliliters of peripheral blood for DNA extraction. Two single nucleotide polymorphisms(SNPs) of CFH(rs1061170 and rs800292) and two SNPs of MAP1LC3B(rs8044820 and rs9903) were genotyped. The genotypes and allele frequencies of the SNPs in the study and control groups were further compared using Chi-square and Fisher’s exact tests. RESULTS: In a high-altitude population, the nominally significant differences of rs800292 and rs9903’s genotype AG frequencies were observed in the AMD group(P=0.034 and 0.004, respectively). The frequencies of allele G of rs800292 and allele A of rs9903 were also significantly dif ferent in the AMD group compared to the control [(P=0.034, OR=0.70, 95%CI: 0.50-0.98) and(P=0.004, OR=1.60, 95%CI: 1.15-2.22), respectively]. No significant differences in the genotype distributions(P=0.16 and 0.40, respectively) and allele frequencies(P>0.05) of rs1061170 and rs8044820 were observed in the AMD group.CONCLUSION: Genotype AG of rs800292 may be a protective factor for AMD. Conversely, rs9903 seems to be a risk factor for AMD. Therefore, allele G of rs800292 may be a protective factor, and allele A of rs9903, a risk factor for AMD in Qinghai high-altitude population.

3H—胸腺嘧啶核苷参入法测定甲亢病人T淋巴细胞功能及其临床意义的初步探讨

本文测定了正常人和四组甲亢病人(n=117)外周血T淋巴细胞(T 细胞)和血清中T_3T_4含量,结果显示:1、四组甲亢病人T淋巴细胞明显低于健康人;2、经抗甲状腺药物治疗后病情缓解、T_3T_4正常、T 细胞功能逐渐恢复;

血清TK1、AFP及CHI3L1预测放疗后原发性肝癌患者预后的临床价值

目的探讨血清胸苷激酶1(TK1)、甲胎蛋白(AFP)、壳多糖酶3样蛋白1(CHI3L1)对放疗后原发性肝癌(PLC)患者预后的预测价值。方法回顾性分析该院2017年1月至2019年6月收治的行立体定向放疗的97例PLC患者的临床资料,根据治疗后1年PLC的复发转移情况将患者分为复发转移组(42例)与未复发转移组(55例)。根据治疗后1年的生存情况将患者分为生存组(67例)、死亡组(30例)。比较复发转移组与未复发转移组、死亡组与生存组的血清TK1、AFP、CHI3L1水平。采用受试者工作特征曲线(ROC曲线)分析血清TK1、AFP及CHI3L1对放疗后PLC患者复发转移及生存情况的预测价值。结果复发转移组血清TK1、AFP、CHI3L1水平均明显高于未复发转移组,差异有统计学意义(P<0.05)。死亡组血清TK1、AFP、CHI3L1水平均明显高于生存组,差异有统计学意义(P<0.05)。ROC曲线分析结果显示,TK1、AFP、CHI3L1联合预测放疗后PLC患者复发转移的AUC为0.847,高于各项指标单独预测。TK1、AFP、CHI3L1联合预测放疗后PLC患者生存情况的AUC为0.936,高于各项指标单独预测。结论血清TK1、AFP、CHI3L1对放疗后PLC患者的预后具有一定的预测价值,可用于临床预后评估。

野生大豆阳离子质子转运体CHX19.3与14-3-3蛋白的相互作用研究

植物14-3-3家族作为蛋白互作的桥梁,在逆境应答过程中发挥重要作用。前期获得了一个野生大豆阳离子质子转运体CHX19.3,其能显著提高耐盐碱性。为进一步揭示CHX19.3调控耐盐碱性的分子机制,研究利用分裂泛素的酵母双杂交系统鉴定了CHX19.3与14-3-3家族蛋白的相互作用。结果显示成功构建了诱饵载体pBT3-STE-GsCHX19.3,GsCHX19.3-Cub-LexAVP16融合蛋白对酵母菌没有毒性,且拓扑结构符合该酵母双杂交系统。Y2H结果发现在检测的10个14-3-3蛋白中,只有GF14f能够与CHX19.3蛋白互作,其余14-3-3蛋白均不存在相互作用。研究表明野生大豆CHX19.3与14-3-3家族蛋白互作具有特异性,为进一步深入研究CHX19.3通过与GF14f互作调控耐盐碱性的分子机理奠定了基础。

湿热处理对花生球蛋白Ara h 3抗原性的影响

为探究湿热处理对花生球蛋白Ara h 3抗原性的影响,采用硫酸铵分级沉淀法从花生脱脂粉中分离纯化出Ara h 3,进行不同温度、时间和质量浓度的湿热处理,通过正交试验确定最优湿热处理条件,采用间接ELISA法检测湿热处理后Ara h 3抗原性变化,测定外源荧光、游离巯基含量以及圆二色光谱,从蛋白结构的变化解释湿热处理对Ara h 3抗原性的影响。研究表明:湿热处理能够降低Ara h 3抗原性,且在质量浓度10 mg/mL、90℃处理30 min时,抗原性降至最低;湿热处理后的Ara h 3荧光强度、表面疏水性增强,三级结构发生变化;游离巯基含量增加、空间结构发生改变;α-螺旋和β-折叠含量降低,无规则卷曲含量增加,二级结构发生变化。湿热处理后Ara h 3空间结构发生改变,部分抗原表位遭到破坏或被包埋,抗原性降低。

壳梭孢素对质膜H^+-ATPase活力影响机制的研究进展

壳梭孢素 (FC)作为一种重要的研究工具广泛用于研究酸介导的生长反应和依赖于质子推动力的膜运输系统 ,FC刺激质膜H+_ATPase的活性是通过FC结合蛋白 (FCBP)与H+_ATPase发生作用。FCBP是 1

Structural insights into a novel histone demethylase PHF8

Dynamic regulation of histone methylation/demethylation plays an important role during development. Mutations and truncations in human plant homeodomain （PHD） finger protein 8 （PHF8） are associated with X-linked mental retardation and facial anomalies, such as a long face, broad nasal tip, cleft lip/cleft palate and large hands, yet its molecular function and structural basis remain unclear. Here, we report the crystal structures of the catalytic core of PHF8 with or without α-ketoglutarate （α-KG） at high resolution. Biochemical and structural studies reveal that PHF8 is a novel histone demethylase specific for di- and mono-methylated histone H3 lysine 9 （H3K9me2/1）, but not for H3K9me3. Our analyses also reveal how human PHF8 discriminates between methylation states and achieves sequence specificity for methylated H3K9. The in vitro demethylation assay also showed that the F279S mutant observed in clinical patients possesses no demethylation activity, suggesting that loss of enzymatic activity is crucial for pathogenesis of PHF8 patients. Taken together, these results will shed light on the molecular mechanism underlying PHF8-associated developmental and neurological diseases.

The therapeutic effect of Jiawei Danshen Decoction on myocardial ischemia-reperfusion injury by inhibiting H_(2)S-mediated autophagy signaling pathway

Objective To investigate the protective effects of Jiawei Danshen Decoction(加味丹参饮,JWDSD)on myocardial ischemia-reperfusion injury(MIRI)via the regulation of serum Hydrogen sulfide(H2S)and cardiac Beclin1,light Chain 3 A/B(LC3 A/B),p62,and autophagy protein5(ATG5).Methods Seventy specific pathogen free(SPF)Sprague-Dawley(SD)rats were randomly assigned to seven groups(n=10 in each group),including normal control,sham operation,MIRI model(model),ischemic preconditioning,Na HS,JWDSD,and JWDSD+CSE inhibitor(JWDSD+PPG)groups,and orally administered the indicated drugs for 14 d.Two hours after the last administration,the left anterior decreased branch of the coronary artery of each rat in model,Na HS,JWDSD,and JWDSD+PPG groups was ligated for 30 min and subsequently reperfused for 90 min to establish the MIRI model,and the rats in the sham operation group were only exposed to the thorax after surgery without coronary ligation.Blood samples were collected to detect H2S levels using an enzyme-linked immunosorbent assay(ELISA).Heart tissues were harvested for histopathological and immunohistochemical examination and quantitative reverse transcription polymerase chain reaction analysis of Beclin1 and ATG5 m RNA expression and Western blot analysis of Beclin1,LC3 A/B,and p62 protein expression.Results(1)The serum H2S content in model group rats was significantly reduced(P<0.01),JWDSD significantly increased the serum H2S content of model group rats(P<0.01),and the CSE inhibitor(PPG)significantly reduced H2S levels in the JWDSD group rats(P<0.01).(2)Compared with the normal control group,the myocardial tissue necrosis and cell destruction occurred in the MIRI model group,and JWDSD could alleviate the myocardial tissue necrosis of model rats,but the ameliorative effect of JWDSD could be reversed by PPG.(3)Beclin1,LC3 A/B,and p62 expression levels in the heart tissues of the model group were significantly increased(P<0.001),whereas decreased by JWDSD(P<0.05,P<0.01,and P<0.001,respectively),and the inhibitory effects of JWDSD on Beclin1,LC3 A/B,and p62 expression were partially reversed by PPG(P<0.01,P<0.05,and P<0.01,respectively).(4)The expression levels of autophagy-related genes Beclin1 and ATG5 were significantly increased in the model group(P<0.001).JWDSD clearly downregulated the expression levels of Beclin1 and ATG5(P<0.05 and P<0.001,respectively),which were reversed by PPG(P<0.001).Conclusion Our experimental data show that JWDSD can exhibit an anti-MIRI role by increasing endogenous H2S generation,and downregulating the expression of Beclin1,LC3 A/B,p62 and ATG5,which are related to inhibiting autophagy signaling.