Cardiovascular disease(CVD)is a major cause of human death and a serious threat to people's health.Therefore,it is very important to explore the early identification,diagnosis and effective treat-ment of CVD.The expression level of microRNA(miRNA)is related to many pathophysiological processes related to CVD,such as myocardial cell metabolism disorder,myocardial cell injury and myocardial fibrosis,which makes miRNA an important entry point for the diagnosis and treatment of CVD.MicroRNA-126(miR-126)is one of the most important biological markers in the miRNA family.It plays a role in protecting the myocardium by participating in angiogenesis,endothelial cell repair,and inhibition of inflammatory responses.This article reviewed the latest research progress on the mechanism,diagnostic significance and potential ther-apeutic value of miR-126 in the occurrence and development of various types of CVD.

Objective To investigate the molecular mechanism of miR-126-EPC-MPs in ameliorating oxygen glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes.Methods The cardiomyocytes were used to establish the control and OGD/R injury models,and EPC-MPs and miR-126 mimic EPC-MPs treatments were administered respectively.The structural changes in cardiomyocyte organelles were assessed by transmission electron microscopy.ELISA was used to detect the expression levels of IL-6,TNF-α and HMGB-1 in cardiomyocytes.The protein and mRNA expression levels of Ang Ⅱ,caspase-6,eNOS,FOXO1,MPO,NF-κB,ERK1,LKB1,SIRT1,GRP78,GM130 and PGC-1α in cardiomyocytes after different treatments were detected by Western blot and quantitative PCR.Results The mitochondria structure in some cardiomyo-cytes of the OGD/R+miR-126 mimic EPC-MPs group was complete,the size of some mitochondria was in-creased,the surface of the endoplasmic reticulum had fewer ribosomes,and some of the Golgi vesicles gath-ered.Compared with the OGD/R+EPC-MPs group,the expression levels of IL-6,TNF-α and HMGB-1 in the OGD/R+miR-126 mimic EPC-MPs group were down-regulated.Compared with the OGD/R+EPC-MPs group,the expression levels of Ang Ⅱ,caspase-6,p-ERK1/2 and GRP78 protein in the OGD/R+miR-126 mimic EPC-MPs group were down-regulated,and the expression levels of p-LKB1,GM130 and PGC-1α protein in the OGD/R+miR-126 mimic EPC-MPs group were up-regulated.The quantitative PCR(qPCR) results showed that compared with the OGD/R+EPC-MPs group,the expression levels of Ang Ⅱ,MPO and GRP78 in the OGD/R+miR-126 mimic EPC-MPs group were down-regulated,and the expression levels of eNOS,GM130 and PGC-1α were up-regulated.Conclusion When OGD/R injury occurs in cardiomyocytes,miR-126 mimic EPC-MPs regulates PGC-1α/GM130 expression and inhibits Ang Ⅱ-induced stress injury response,thereby reduces the OGD/R damage in cardiomyocytes.

Objective To study the diagnostic value of miR-126 and ICAM-1 in peripheral blood endo-thelial microparticles(EMPs)of the patients with acute myocardial infarction(AMI).Methods A total of 45 patients with definitely diagnosed AMI in this hospital from September 2021 to June 2022 were selected as the AMI group.Other 45 healthy subjects in the same age group and sex were selected as the control group.Be-fore coronary angiography,the patient's peripheral blood was collected,and the flow cytometry was used to conduct the qualitative and quantitative analysis on EMPs.The expression levels of miR-126 and ICAM-1 in EMPs were determined by using fluorogenic quantitative PCR and ELISA.The receiver operating characteristic(ROC)curve was adopted to evaluate the diagnostic value of the related indicators for AMI.Results There was no statistically significant difference in the general data such as age,gender and BMI between the two groups(P＞0.05).The biochemical indicators such as PLT,BUN,TC,TG and HDL-C had no statistical difference between the two groups(P＞0.05).The expression level of miR-126 in the AMI group was significantly lower than that in the control group,the expression level of ICAM-1 in the AMI group was higher than that in the control group,and the differences were not statistically significant(P＜0.05).The miR-126 expression level in the AMI group was lower than that in the control group,the ICAM expression level was higher than that in the control group,and the differences were statistically significant(P＜0.05).The multivariate logistic regression results showed that miR-126,ICAM-1 and CK-MB had the independent correlation with the AMI occurrence(P＜0.05).The area under the curve(AUC)of mir-126 for diagnosing AMI was 0.813(95％CI:0.725-0.903,P＜0.001),which of ICAM-1 was 0.848(95％CI:0.764-0.933,P＜0.001),and which of miR-126 and ICAM-1 combination diagnosis was 0.922(95％CI:0.870-0.946,P＜0.001).Conclusion The miR-126 and ICAM-1 expression levels in EMPs have the independent correlation with AMI,and the both have the di-agnostic value for AMI.

Objective To investigate the effects of endothelial progenitor cells(EPC)-derived microp-articles(MPs)with different injury treatments on EPC.Methods EPC cells were cultured and EPCs were i-dentified by flow cytometry.EPCs were treated with high glucose(HG)and tumor necrosis factor(TNF)-a recombinant protein,and MPs were extracted.The structural changes of microtubules,Golgi bodies and other organelles in EPC were observed by transmission electron microscopy.MTT assay was used to detect cell pro-liferation.Cell scratch assay was used to evaluate cell migration ability.Cell lumen formation assay was used to detect lumen formation.The expression levels of endothelial nitric oxide synthase(eNOS),silent informa-tion regulator 1(SIRT1),rat sarcoma(RAS)and extracellular regulated protein kinase(ERK)in EPC after different treatments were detected by quantitative real-time fluorescence PCR(qPCR)and Western blot.Re-sults Compared with the control-EPC-MPs group,the microtubule structure of the HG-EPC-MPs group and the TNF-α-EPC-MPs group was complete,the length was shortened,and the Golgi structure was relatively complete.Compared with the control-EPC-MPs group,the proliferation rate of EPC in the HG-EPC-MPs group and the TNF-α-EPC-MPs group was down-regulated,the cell migration ability was decreased,and the tube formation was decreased(P＜0.05).Compared with the control-EPC-MPs group,the mRNA and protein expressions of eNOS,SIRT1,RAS and ERK in the HG-EPC-MPs group and the TNF-α-EPC-MPs group were down-regula-ted(P＜0.05).Conclusion HG and TNF-α mediated MPs derived from EPC injury may change the structure of organelles in EPC by regulating the expression of SIRT1/ERK1 pathway proteins,thus affecting the biolog-ical function of EPC.

OBJECTIVE：To investiga te the effects of MEK/ERK pathway specific inhibitor PD 98059 combined with paclitaxel on the proliferation and apoptosis of human gastric signet ring cell carcinoma （SRCC）cells. METHODS ：Using human SRCC KATO Ⅲ cells as object ，CCK-8 assay was used to detect cell proliferation after treated with paclitaxel ，PD98059 and two drug combination for 48 h，and the proliferation rate was calculated. Flow cytometry ，Western blotting and Transwell assay were used to detect the cell proliferation ，the expression of apoptosis related protein （Cleaved-caspase-3）and cell migration after treated with paclitaxel，PD98059 and two drug combination for 48 or 24 h. RESULTS ：After treated with paclitaxel （1 μg/mL），PD98059（5， 20，40 μmol/L）and two drug combination （1 μg/mL+5，20，40 μmol/L），the proliferation rate of cells was increased significantly in administration groups ，and the combination groups were significantly higher than paclitaxel and PD 98059 alone groups （P＜ 0.05）. After treated with paclitaxel （1 μg/mL），PD98059（5，20，40 μmol/L）and two drug combination （1 μg/mL+40 μmol/L）， early and late apoptosis rate ，the protein expression of Cleaved-caspase- 3 were significantly increased in paclitaxel group and combination group ；combination group was significantly higher than paclitaxel and PD 98059 alone group （P＜0.05）. The number of migrated cells in administration groups were reduced significantly ，and the combination group was significantly lower than paclitaxel and PD 98059 alone group （P＜0.05）. CONCLUSIONS ：Paclitaxel and PD 98059 can inhibit the proliferation and migration of human SRCC KATO Ⅲ cells，paclitaxel can also promote the apoptosis and the expression of apoptosis related protein，which may be related to the inhibition of MEK/ERK pathway. The effect of the combination of the two drugs is better than paclitaxel or PD 98059 alone.

Objective: To study the effect of miR-340-5p on the proliferation of laryngeal cancer Hep2 cells and explore its intrinsic molecular mechanism, so as to screen potential biomarkers and targets for the diagnosis and treatment of laryngeal cancer. Method: The expression of miR-340-5p in laryngeal cancer tissues, paracancerous tissues, laryngeal cancer cell lines Hep2 and normal bronchial HBE cell lines was quantitatively analyzed by qRT-PCR; The double luciferase reporter vector was constructed to verify whether STAT3 was a potential target gene of microRNA-340-5p; The miR-340-5p mimics/inhibitor was transfected into Hep2 cells by liposome and verified by qRT-PCR; The CCK-8 method and Annexin V/PI method were used to analyze the proliferation and apoptosis of transfected cells; and Western Blot was used to detect the expression of STAT3 and Wnt/β-catenin pathway-related proteins after transfection. Result: The results of qRT-PCR showed that the level of miR-340-5p in laryngeal cancer tissues and Hep2 cells was significantly lower than that in adjacent tissues and HBE cells, and the expression of miR-340-5p was significantly increased or decreased after overexpression or inhibition; Luciferase activity showed that miR-340-5p directly interacted with target gene STAT3 3'-UTR and negatively regulated its expression; Cell proliferation and apoptosis analysis showed that up-regulation of microRNA-340-5p could significantly inhibit the proliferation and induce apoptosis of Hep2 cells in vitro, and vice versa; Western Blot results showed that the levels of STAT3 and β-catenin, c-Myc, TCF-4, CyclinD1 and ROCK1 in Hep2 cells were significantly lower than those in the control group after over-expression of miR-340-5p, and vice versa. Conclusion The expression of miR-340-5p is abnormally low in laryngeal cancer tissues and Hep2 cells. It can be used as a potential biological target for diagnosis and treatment of laryngeal cancer by targeting STAT3 gene to negatively regulate Wnt/β-catenin signaling pathway.

To study the effect of miR-340-5p on the proliferation of laryngeal cancer Hep2 cells and explore its intrinsic molecular mechanism, so as to screen potential biomarkers and targets for the diagnosis and treatment of laryngeal cancer. The expression of miR-340-5p in laryngeal cancer tissues, paracancerous tissues, laryngeal cancer cell lines Hep2 and normal bronchial HBE cell lines was quantitatively analyzed by qRT-PCR; The double luciferase reporter vector was constructed to verify whether STAT3 was a potential target gene of microRNA-340-5p; The miR-340-5p mimics/inhibitor was transfected into Hep2 cells by liposome and verified by qRT-PCR; The CCK-8 method and Annexin V/PI method were used to analyze the proliferation and apoptosis of transfected cells; and Western Blot was used to detect the expression of STAT3 and Wnt/β-catenin pathway-related proteins after transfection. The results of qRT-PCR showed that the level of miR-340-5p in laryngeal cancer tissues and Hep2 cells was significantly lower than that in adjacent tissues and HBE cells, and the expression of miR-340-5p was significantly increased or decreased after overexpression or inhibition; Luciferase activity showed that miR-340-5p directly interacted with target gene STAT3 3'-UTR and negatively regulated its expression; Cell proliferation and apoptosis analysis showed that up-regulation of microRNA-340-5p could significantly inhibit the proliferation and induce apoptosis of Hep2 cells in vitro, and vice versa; Western Blot results showed that the levels of STAT3 and β-catenin, c-Myc, TCF-4, CyclinD1 and ROCK1 in Hep2 cells were significantly lower than those in the control group after over-expression of miR-340-5p, and vice versa. The expression of miR-340-5p is abnormally low in laryngeal cancer tissues and Hep2 cells. It can be used as a potential biological target for diagnosis and treatment of laryngeal cancer by targeting STAT3 gene to negatively regulate Wnt/β-catenin signaling pathway.

Objective To investigate the expression of malondialdehyde ( MDA) in esophageal mu-cosa of different types of gastroesophageal reflux disease ( GERD) patients and its role in the esophageal in-flammation. Methods According to the inclusion and exclusion criteria, 42 patients hospitalized in the the Xinjiang Uygur Autonomous Region People's Hospital from December 2017 to October 2018 were selected as the research group. 8 healthy subjects completed physical examination were set up as healthy control group. GERD completed GERDQ score, 24 h pH monitoring, and taken 3 cm on the dentate line of the esophagus as a specimen. The study group was divided into non-erosive reflux disease (NERD) group (17 cases) and Ero-sive reflux disease [erosive esophagitis (RE)] group (25 cases). Then hematoxylin-eosin (HE) staining, immunohistochemistry, real-time polymerase chain reaction ( qPCR ) , enzyme-linked immunosorbent assay (ELISA) methods were used to detect inflammation, oxidative stress (MDA), antioxidant enzyme [manga-nese superoxide dismutase (Mn SOD), glutathione (GSH), catalase (CAT)], and proinflammatory cyto-kines [monocyte chemotactic protein-1 (MCP-1), interlukin-8 (IL-8), tumor necrosis factorα(TNF-α)]. Results There was no significant difference in body mass index ( BMI ) between the three groups ( P >0. 05). 24 h pH monitoring of esophagus showed that the indexes of weak acid reflux (40. 05). In RE group , the infiltration of immune cells (neutrophils, eosinophils), nipple lengthening, edema and other inflammatory changes were found in the esophageal mucosa, and the inflammation score reached the peak, which was signif-icantly higher than that in NERD group, with statistical significant difference (P<0. 001). The positive ex-pression of MDA in the two groups ( NERD, RE) was higher than that in the control group, and the MDA ex-pression in the RE group was almost covered with the full layer esophagus. The serum MDA concentration in the NERD and RE groups was significantly higher than that in the control group (P<0. 001). Compared with the NERD group, the serum MDA in the RE group reached the peak (P<0. 01). The relative expression of mRNA ( Mn SOD, GSH and CAT) in NERD group and RE group was significantly decreased, and there was a significant difference between the three groups (P<0. 001). Compared with the NERD group, the mRNA expression level of Mn SOD and CAT in RE group was significantly decreased (P<0. 01). The relative ex-pression of mRNA (MCP-1, IL-8, TNF- α) increased significantly in the two groups (NERD, RE), and there was a statistically significant difference between the three groups ( P <0. 001 ) . Compared with the NERD group, the expression of its inflammatory factors in the RE group significantly increased (P<0. 01). Conclusions The expression level of MDA in different types of GERD is significantly higher, which may be closely related to esophageal inflammation induced by acid reflux.

Objective To investigate the prevalence of BRCA1/2 gene mutations among Uygur and Han sporadic breast cancer patients in Xinjiang Uygur Automous.Methods Polymerase chain reaction ( PCR) and DNA se-quencing was used to detect mutations of BRCA1(exons 2, 11(11A and 11B) and 20) and BRCA2(exon 11) genes in the Paraffin imbedding tissues from 230 sporadic breast cancer patients ( 115 Uygur and 115 Han ) in Xinjiang Uygur Automous.Results In the 230 cases of sporadic breast cancer patients, 16 cases have gene mu-tation ( 16/230 ,6.96%) .One case of BRCA1 gene in 16 cases of mutations -5 382 locus mutation and 7 cases of new mutations.There was 2 germline mutation in exon 11 of BRCA2 gene.BRCA gene mutation rates of Uygur and Han patients were 7.83% ( 9/115 ) and 6.09% ( 7/115 ) .The onset age of mutations group were 50 or less.Mutations group of patients with amenorrhea ( 3 ) were less than whom were premenopausal ( 13 ) ( P <0.05 ) .Conclusions The prevalence of BRCA1 mutations was significantly higher than BRCA2 in sporadic breast cancer patients of Xinjiang.

Objective To investigate the protective effect and mechanism of Klotho protein on oxidative stress in renal tubular epithelial cells of experimental rat nodels of renal calcium oxalate stone.Methods The 30 SD rats,6-8 weeks old,were randomly divided into 3 groups (10 of each),normal control group(group A),calcium oxalate model group(group B),drug plus calcium oxalate model group (group C).Group A was established with physiological saline by garage each day,group B was established with 1％ ethylene glycol in drinking water + 2％ ammonium chloride by garage (2 ml/d),group C was established with Fosinopril 2.5mg + Valsartan 15mg aqueous solution 2 ml by gavage on the basis of group B (2 ml/d).4 weeks later,the level of malondialdehyde (MDA),superoxide dismutase (SOD),catalase (CAT) and glutathione peroxidase (GSH) in the kidney homogenate were measured by double antibody sandwich enzyme-linked immunosorbent assay (ELISA),Polymerase chain reaction (RT-PCR) was used to measure expression of Klotho and Nrf2 mRNA,and Western Blot was used to measure the expression of Klotho and Nrf2 protein.Results The level of MDA in group B [(12.43 ± 0.43) μmol/mg] was significantly increased compared to group A[(8.67 ±0.84) μmol/mg,P ＜0.05] and group C [(7.97 ±0.81) μmol/mg,P＜0.05],while group A was close to group C (P ＞0.05).In group A,B,and C,the levels of SOD were (247.89 ± 2.45),(109.54 ± 4.21),and (189.74 ± 10.47) U/mg,respectively;the levels of GSH were (38.98 ± 4.55),(26.87 ± 3.92),and (31.29± 2.54) μmol/mg,respectively;CAT were (138.47 ± 8.74),(119.87 ± 8.45),and (127.46 ± 7.45) U/mg,respectively.The levels of SOD,GSH,CAT in group B were significantly lower than that in group A and C,while those in group B were close to group A (P ＞ 0.05).The expression of Klotho and Nrf2 mRNA in group B [(0.208 ± 0.036) and (0.499 ± 0.086)] were significantly lower than group A (1.011 ± 0.174 and 1.023 ± 0.139,P ＜ 0.05)and group C(1.123 ±0.248 and 1.023 ±0.139,P ＜0.05).The expression of Klotho and Nrf2 protien were also significantly lower than that in group A and C (P ＜0.05).Conclusions Valsartan and Fosinopril could prevent the formation of renal CaOx stones by upregulating expression of low level Klotho gene induced by ethylene glycol.This effect may be involved with activation of Keapl-Nrf2-ARE signaling pathway.