AIM: To investigate the expression and effects of sialyl Lewis X (SLeX) on the invasion and migration of human hepatocellular carcinoma HepG2 cells.METHODS: The expression of α1,3-fucosyltransferase VII (FUT7) in HepG2 cells and L-02 cells was detected by RT-qPCR and Western blot.The SLeX expression in HepG2 cells and L-02 cells was determined by Western blot and immunocytochemical staining.The invasion and migration abilities of the treated cells were evaluated by Transwell assay.RESULTS: The expression of FUT7 and SLeX in the HepG2 cells, but not in the L-02 cells, was observed.The invasion rates of the HepG2 cells treated with SLeX monoclonal antibody at 0.05, 0.5 and 5 mg/L were significantly decreased as compared with control group (P<0.05).The migration ability of the HepG2 cells treated with SLeX monoclonal antibody at 0.05, 0.5 and 5 mg/L was also significantly reduced as compared with control group (P<0.05).The invasion rate and migratory cell number were significantly different between any 2 groups in the HepG2 cells treated with SLeX monoclonal antibody at 0.05, 0.5 and 5 mg/L (P<0.05).CONCLUSION: HepG2 cells express SLeX.SLeX is closely related to the migration and invasion abilities of the HepG2 cells.

Objective: To explore the relationship between blood levels of cyclophilin A (CyPA) and chronic heart failure (CHF).
Methods: A total of 166 CHF patients were enrolled as CHF group, according to NYHA classiifcation, it was further divided into 4 sub-groups: Class I,n=37, Class II,n=39, Class III,n=46 and Class IV,n=44. In addition, there was a Normal control group,n=52. Blood levels of CyPA, B-type natriuretic peptide (BNP) and high sensitivity C-reactive protein (hs-CRP) were examined and compared among different groups.
Results: Compared with Normal control group, CHF group had elevated CyPA (5.11 ± 2.43) ng/ml vs (2.28 ± 0.61) ng/ml, BNP (385.65 ± 184.06) pg/ml vs (90.37 ± 18.44) pg/ml and hs-CRP (11.74 ± 5.44) mg/L vs (5.99 ± 1.14) mg/L, all P<0.05. As increased severity of NYHA classiifcation, blood levels of CyPA, BNP and hs-CRP between 2 subgroups had the increasing trend accordingly, allP<0.05; while there was an exception: blood levels of CyPA and hs-CRP were similar between Class I subgroup and Normal control group, allP>0.05. Pearson correlation analysis indicated that blood levels of CyPA were positively related to BNP and hs-CRP in CHF patients (r=0.838,P<0.01 and r=0.755,P<0.01).
Conclusion: Blood levels of CyPA were elevated in CHF patients and it’s obviously related to NYHA classiifcation, which might have certain effects on CHF diagnosis and evaluation.

Aim To observe whether the activation of aldehyde dehydrogenase 2 ( ALDH2 ) can protect a-gainst diabetes induced liver injury in rat model, and analyze the role of JNK pathway in the liver protection induced by activation of ALDH2 . Methods All male SD rats were randomly divided into three groups: nor-mal control group ( Con ) , diabetes group ( DM ) and ethanol + diabetes group ( EtOH + DM ) . After 8 weeks, the fasting blood glucose ( FBG) level, glyco-sylated hemoglobin ( HbA1c) level, serum AST and ALT levels were measured. The changes of hepatic pa-thology were observed by hematoxylin and eosin ( HE) staining method. The protein expressions of ALDH2, JNK and p-JNK in liver tissue were measured. Result Compared with control group, in DM group, the lev-els of FBG and HbA1c, serum AST and ALT levels were increased significantly. The structure of liver mor-phology was destroyed, disarranged and unclear, the hepatocyte was swollen, and a large number of inflam-matory cells were infiltrated. ALDH2 protein expres-sion was decreased, while the expressions of JNK, p-JNK and the ratio of p-JNK/JNK were increased. Com-pared with DM group, in EtOH+DM group, the levels of FBG and HbA1c, serum AST and ALT levels were decreased. The expression of ALDH2 protein was in-creased, accompanying with the decrease of JNK, p-JNK protein expressions and the ratio of p-JNK/JNK. Conclusion Activation of ALDH2 can protect the liv-er against diabetes induced liver damage in rat model, which may be relevant with inhibiting the JNK path-way.

OBJECTIVETo investigate the correlation of G487A polymorphism of aldehyde dehydrogenase-2 (ALDH2) gene with hypertension in patients with coronary heart disease complicated by type 2 diabetes.

METHODSThis study was conducted among 167 patients with coronary heart disease complicated by diabetes mellitus. The polymorphisms of gene G487A ALDH2 were determined using polymerase chain reaction-restricted fragments length polymorphism technique (PCR-RFLP). According to the genotypes, the patients were divided into GG group (n=105) and GA/AA group (n=62), and the incidence of hypertension, risk factors of hypertension, systolic and diastolic pressures, and pulse pressure indexes were compared between the two groups. Multivariate logistic regression analysis was performed to adjust the effects of the confounding factors.

RESULTSThe incidence of hypertension in GA/AA group was significantly higher than that in GG group (P<0.05), and the former group showed a significantly greater differences between systolic and pulse pressure; the diastolic pressure was comparable between the two groups. Multivariate logistic regression analysis showed that GA/AA was associated with an increased risk of hypertension in synergy with high insulin level and insulin resistance.

CONCLUSIONALDH2 gene G487A polymorphism may be associated with hypertension in patients with coronary heart disease complicated by type 2 diabetes, and the patients with an A allele have a greater risk of developing hypertension.

Aged ; Alcohol Dehydrogenase ; genetics ; Coronary Disease ; complications ; genetics ; Diabetes Mellitus, Type 2 ; complications ; genetics ; Female ; Humans ; Hypertension ; etiology ; Male ; Middle Aged ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Risk Factors

Objective To explore the effect of quercetin on renal inflammation and cell apoptosis in diabetic rats and its possible mechanisms.Methods Twenty-four adult male SD rats were randomized equally into normal control group,high-glucose and high-fat feeding group,streptozotocin(STZ)-induced diabetic model group,and quercetin treatment(daily dose 100 mg/kg)group.Pathological changes of the renal tissues of the rats were observed with HE staining,serum inflammatory factor levels were determined with ELISA,and renal expression of NF-κB was observed by immunohistochemistry.Fast blood glucose(FBG),serum levels of triglyceride(TG),BUN,and Scr,and 24-h urine protein content of the rats were measured,and renal expressions of HMGB1,RAGE,NF-κB,Bax,Bcl-2,and caspase-3 were detected with Western blotting.Results The diabetic rats showed significantly increased levels of FBG,TG,BUN,and Scr,renal hypertrophy index,24-h urinary protein content,serum IL-1β,IL-6 and TNF-α levels and renal expressions HMGB1,RAGE,NF-κB,Bax,and caspase-3 with decreased renal expression of Bcl-2.All these changes were significantly alleviated by quercetin treatment of the rats.Conclusion Quercetin can ameliorate kidney injury in diabetic rats possibly by inhibiting the HMGB1/RAGE/NF-κB inflammatory signaling pathway to reduce renal inflammation and renal cell apoptosis.

Objective To explore the effect of quercetin on renal inflammation and cell apoptosis in diabetic rats and its possible mechanisms.Methods Twenty-four adult male SD rats were randomized equally into normal control group,high-glucose and high-fat feeding group,streptozotocin(STZ)-induced diabetic model group,and quercetin treatment(daily dose 100 mg/kg)group.Pathological changes of the renal tissues of the rats were observed with HE staining,serum inflammatory factor levels were determined with ELISA,and renal expression of NF-κB was observed by immunohistochemistry.Fast blood glucose(FBG),serum levels of triglyceride(TG),BUN,and Scr,and 24-h urine protein content of the rats were measured,and renal expressions of HMGB1,RAGE,NF-κB,Bax,Bcl-2,and caspase-3 were detected with Western blotting.Results The diabetic rats showed significantly increased levels of FBG,TG,BUN,and Scr,renal hypertrophy index,24-h urinary protein content,serum IL-1β,IL-6 and TNF-α levels and renal expressions HMGB1,RAGE,NF-κB,Bax,and caspase-3 with decreased renal expression of Bcl-2.All these changes were significantly alleviated by quercetin treatment of the rats.Conclusion Quercetin can ameliorate kidney injury in diabetic rats possibly by inhibiting the HMGB1/RAGE/NF-κB inflammatory signaling pathway to reduce renal inflammation and renal cell apoptosis.

Objective To analyze the correlation of copper death inducer ferredoxin 1(FDX1)and lipoic acid(LA)with the occurrence and severity of coronary atherosclerosis and explore their roles in coronary heart disease(CHD).Methods We analyzed the data of 226 patients undergoing coronary artery angiography(CAG)in our hospital between October,2021 and October,2022,including 47 patients with normal CAG findings(control group)and 179 patients with mild,moderate or severe coronary artery stenosis(CHD group).Serum FDX1 and LA levels were determined with ELISA for all the patients.We also examined pathological changes in the aorta of normal and ApoE-/-mice using HE staining and observed collagen fiber deposition with Sirius red staining.Immunohistochemistry was used to detect the expression and distribution of FDX1 and LA in the aorta,and RT-PCR was performed to detect the expressions of FDX1,LIAS and ACO2 mRNAs in the myocardial tissues.Results Compared with the control patients,CHD patients had significantly lower serum FDX1 and LA levels,which decreased progressively as coronary artery stenosis worsened(P<0.01)and as the number of involved coronary artery branches increased(P<0.05).Serum FDX1 and LA levels were positively correlated(r=0.451,P<0.01)and they both negatively correlated with the Gensini score(r=-0.241 and-0.273,respectively;P<0.01).Compared with normal mice,ApoE-/-mice showed significantly increased lipid levels(P<0.01)and atherosclerosis index,obvious thickening,lipid aggregation,and collagen fiber hyperplasia in the aorta,and significantly reduced expressions of FDX1,LA,LIAS,and ACO2(P<0.05).Conclusion Serum FDX1 and LA levels decrease with worsening of coronary artery lesions,and theirs expressions are correlated with coronary artery lesions induced by hyperlipidemia.

Objective To explore the impact of diabetes on collateral circulation (CC) development in patients with chronic total coronary occlusion (CTO) and the underlying regulatory mechanism. Methods This study was conducted among 87 patients with coronary heart disease (CHD), who had CTO in at least one vessel as confirmed by coronary angiography. Among them 42 patients were found to have a low CC level (Cohen-Rentrop grades 0-1) and 45 had a high CC level (grades 2-3). In the 39 patients with comorbid diabetes mellitus and 48 non-diabetic patients, insulin resistance (IR) levels were compared between the subgroups with different CC levels. The steady-state mode evaluation method was employed for calculating the homeostatic model assessment for insulin resistance index (HOMA-IR) using a mathematical model. During the interventional procedures, collateral and peripheral blood samples were collected from 22 patients for comparison of the metabolites using non-targeted metabolomics analysis. Results NT-proBNP levels and LVEF differed significantly between the patients with different CC levels (P<0.05). In non-diabetic patients, HOMA-IR was higher in low CC level group than in high CC level groups. Compared with the non-diabetic patients, the diabetic patients showed 63 upregulated and 48 downregulated metabolites in the collateral blood and 23 upregulated and 14 downregulated metabolites in the peripheral blood. The differential metabolites in the collateral blood were involved in aromatic compound degradation, fatty acid biosynthesis, and steroid degradation pathways; those in the peripheral blood were related with pentose phosphate metabolism, bacterial chemotaxis, hexanoyl-CoA degradation, glycerophospholipid metabolism, and lysine degradation pathways. Conclusion The non-diabetic patients with a low level of CC had significant insulin resistance. The degradation pathways of aromatic compounds, fatty acid biosynthesis, and steroid degradation are closely correlated with the development of CC.

Objective To analyze the correlation of copper death inducer ferredoxin 1(FDX1)and lipoic acid(LA)with the occurrence and severity of coronary atherosclerosis and explore their roles in coronary heart disease(CHD).Methods We analyzed the data of 226 patients undergoing coronary artery angiography(CAG)in our hospital between October,2021 and October,2022,including 47 patients with normal CAG findings(control group)and 179 patients with mild,moderate or severe coronary artery stenosis(CHD group).Serum FDX1 and LA levels were determined with ELISA for all the patients.We also examined pathological changes in the aorta of normal and ApoE-/-mice using HE staining and observed collagen fiber deposition with Sirius red staining.Immunohistochemistry was used to detect the expression and distribution of FDX1 and LA in the aorta,and RT-PCR was performed to detect the expressions of FDX1,LIAS and ACO2 mRNAs in the myocardial tissues.Results Compared with the control patients,CHD patients had significantly lower serum FDX1 and LA levels,which decreased progressively as coronary artery stenosis worsened(P<0.01)and as the number of involved coronary artery branches increased(P<0.05).Serum FDX1 and LA levels were positively correlated(r=0.451,P<0.01)and they both negatively correlated with the Gensini score(r=-0.241 and-0.273,respectively;P<0.01).Compared with normal mice,ApoE-/-mice showed significantly increased lipid levels(P<0.01)and atherosclerosis index,obvious thickening,lipid aggregation,and collagen fiber hyperplasia in the aorta,and significantly reduced expressions of FDX1,LA,LIAS,and ACO2(P<0.05).Conclusion Serum FDX1 and LA levels decrease with worsening of coronary artery lesions,and theirs expressions are correlated with coronary artery lesions induced by hyperlipidemia.

Objective To explore the impact of diabetes on collateral circulation (CC) development in patients with chronic total coronary occlusion (CTO) and the underlying regulatory mechanism. Methods This study was conducted among 87 patients with coronary heart disease (CHD), who had CTO in at least one vessel as confirmed by coronary angiography. Among them 42 patients were found to have a low CC level (Cohen-Rentrop grades 0-1) and 45 had a high CC level (grades 2-3). In the 39 patients with comorbid diabetes mellitus and 48 non-diabetic patients, insulin resistance (IR) levels were compared between the subgroups with different CC levels. The steady-state mode evaluation method was employed for calculating the homeostatic model assessment for insulin resistance index (HOMA-IR) using a mathematical model. During the interventional procedures, collateral and peripheral blood samples were collected from 22 patients for comparison of the metabolites using non-targeted metabolomics analysis. Results NT-proBNP levels and LVEF differed significantly between the patients with different CC levels (P<0.05). In non-diabetic patients, HOMA-IR was higher in low CC level group than in high CC level groups. Compared with the non-diabetic patients, the diabetic patients showed 63 upregulated and 48 downregulated metabolites in the collateral blood and 23 upregulated and 14 downregulated metabolites in the peripheral blood. The differential metabolites in the collateral blood were involved in aromatic compound degradation, fatty acid biosynthesis, and steroid degradation pathways; those in the peripheral blood were related with pentose phosphate metabolism, bacterial chemotaxis, hexanoyl-CoA degradation, glycerophospholipid metabolism, and lysine degradation pathways. Conclusion The non-diabetic patients with a low level of CC had significant insulin resistance. The degradation pathways of aromatic compounds, fatty acid biosynthesis, and steroid degradation are closely correlated with the development of CC.