Animals ; Apoptosis ; Bradykinin ; metabolism ; Bradykinin Receptor Antagonists ; Ischemia ; metabolism ; Ischemic Preconditioning ; Muscle, Skeletal ; blood supply ; metabolism ; pathology ; Myocardial Infarction ; metabolism ; Myocardium ; pathology ; Swine ; Swine, Miniature

AIM:To evaluate 23G vitrectomy for macular edema in eyes with retinal vein occlusion (RVO) combined with vitreoretinal traction (VMT) or epiretinal membrane (ERM).METHODS:Totally 22 patients (22 eyes) diagnosed with macular edema of RVO combined with VMT or ERM were retrospectively analyzed.Twelve cases performed with 23G vitrectomy together with peeling of inner limiting membrane (ILM) and/or ERM were considered as the observation group or intervention group.Ten cases without vitrectomy were recruited as control group.The best corrected visual acuity (BCVA) and central retinal thickness (CRT) at baseline, 1, 3 and 6mo were recorded and compared.RESULTS:At baseline, the difference of BCVA and CRT between observation group and control group was not statistically significant (P=0.645, 0.206).After vitrectomy, the BCVA and CRT of RVO patients in observation group were significantly improved compared with baseline at each follow-up (F=2.895, P=0.048;F=16.431, P<0.01).However, the BCVA and CRT in control group remained the same as baseline at every follow-up.Moreover, the BCVA and CRT in observation group were much better than that in control group at both 3 and 6mo after vitrectomy.However, the BCVA and CRT between two groups were not significantly different at 1mo postoperatively.CONCLUSION:The 23G vitrectomy could markedly improve BCVA and reduce CRT in RVO patients with macular edema combined with VMT and/or ERM.

Objective To evaluate the role of the mitochondrial ATP-sensitive potassium (mito-KATP)channel in sevoflurane preconditioning-induced delayed cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts.Methods Seventy-two adult male Sprague-Dawley rats were randomly divided into 6 groups (n =12 each):control group (group CON),I/R group,sevoflurane control group (group SEVO),sevoflurane preconditioning group (group SWO P),5-hydroxydeconoate (5-HD) + sevoflurane preconditioning group (group 5-HD+ SWOP) and 5-HD control group (group 5-HD).The rats were exposed to 33％ pure oxygen for 1 h in groups CON and I/R.The rats were exposed to 2.5％ sevoflurane for 1 h in groups SEVO and SWOP.5-HD (a mito-KATP channel inhibitor) 10 mg/kg was injected intraperitoneally 30 min before sevoflurane preconditioning in group 5-HD + SWOP.5-HD 10 mg/kg was injected intraperitoneally in group 5-HD.The hearts were immediately removed and perfused in a Langendorff apparatus.The hearts were made globally ischemic for 30 min followed by 120 min reperfusion in groups I/R,SWOP,5-HD + SWOP and 5-HD.The expression of phosphorylated protein kinase C-epsilon (p-PKC-ε) and caspase-8 was measured by Western blot immediately before ischemia (T0) and at 120 min of reperfusion (T1).The myocardial infarct volume was measured by TTC staining.Results Compared with group CON,the myocardial infarct volume was significantly increased at T1 in groups I/R,SWOP,5-HD +SWOP and 5-HD,p-PKC-ε expression was up-regulated at T0 in groups SEVO and SWOP and at T1 in groups I/R,SWOP,5-HD + SWOP and 5-HD,and caspase-8 expression was down-regulated at T1 in group SEVO (P ＜0.05).Compared with group I/R,the myocardial infarct volume was significantly decreased at T1 in groups SWOP and 5-HD + SWOP,p-PKC-ε expression was up-regulated at T0 in groups SEVO and SWOP,and caspase-8 expression was down-regulated at T1 in group SWOP (P ＜ 0.05).Compared with group SWOP,the myocardial infarct volume was significantly increased,p-PKC-ε expression was down-regulated at T0,and caspase-8 expression was up-regulated at T1 in group 5-HD + SWOP (P ＜ 0.05).Conclusion The mito-KATP channel is involved in sevoflurane preconditioning-induced delayed cardioprotection against I/R injury in isolated rat hearts through upregulation of p-PKC-ε expression before ischemia and inhibition of cell apoptosis during reperfusion.

AIM: To explore the role of phosphatidylinositiol 3-kinase/protein kinase B/endothelial nitric oxide synthase (PI3K/Akt/eNOS) signaling pathways in the inhibitory effects of puerarin on oxidized low-density lipoprotein (ox-LDL)-induced tissue factor (TF) expression in vascular endothelial cells.METHODS: The mRNA expression of TF was detected by real-time fluorescent quantitative PCR.The protein levels of TF and Akt was determined by Western blot.The content of the nitric oxide (NO) was measured by nitrate reduction method.RESULTS: Compared with control group, incubating endothelial cells with ox-LDL significantly induced TF expression at mRNA and protein levels and the dephosphorylation of Akt protein, and decreased NO production.Incubation of the endothelial cells with puerarin for 1 h and then treatment of the cells with ox-LDL decreased the TF expression at mRNA and protein levels, increased Akt protein phosphorylation and intracellular NO content.Co-incubation of the endothelial cells with PI3K inhibitor LY294002 and puerarin for 1 h and then treatment of the cells with ox-LDL augmented the TF expression at mRNA and protein levels and the Akt protein dephosphorylation, and decreased NO production.Co-incubation of the endothelial cells with eNOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and puerarin significantly decreased the inhibitory effect of puerarin on ox-LDL-induced TF expression at mRNA and protein levels in the endothelial cells, and reduced Akt protein phosphorylation and NO production.CONCLUSION: Puerarin inhibits ox-LDL-induced TF expression at mRNA and protein levels in the human umbilical vein endothelial cells via activation of PI3K/Akt/eNOS signaling pathway.

Objective To investigate the effects of puerarin on the expression of human umbilical vein endothelial cells (HUVECs) tissue factor (TF) and tissue factor pathway inhibitor (TFPI) induced by oxidized low-density lipoprotein (ox-LDL).Methods After HUVECs were incubated with different concentrations of puerarin and 50 mg/L ox-LDL,the expression of TF and TFPI mRNA and protein were detected by real-time fluorescent quantitative PCR and Western blot respectively.Results Compared with control,treatment with ox-LDL caused the augment of TF mRNA and protein expression (P<0.01),and the decrease of TFPI mRNA and protein expression.However,50,100,and 200 μmol/L puerarin blunted the augment of TF mRNA and protein expression and weakened the inhibition of TFPI mRNA and protein expression induced by ox-LDL(P<0.01).Conclusions Puerarin reduces HUVECs TF and TFPI mRNA and protein induced by ox-LDL.

Objective To identify the differential serum proteins in patients with hepatic injury resulting from coal-burning type of arsenism. Methods Six serum samples were collected from patients with liver injury resulting from coal-burning type of arsenism and healthy subjects(control gruop) in endemic arsenism area. Twodimensional gel electrophoresis(2-DE) was performed to separate serum proteins, after silver staining, the differential expression of proteins were analyzed and then identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry(MALDI-TOF-MS). Results The 2-DE map of serum protein patterns of patients and normal control were established successfully. The results showed that there were an average of (824 ± 31 ) spots and (782 ± 42) spots on 2-DE matching of the patients and control groups and the matching rate was 94.9%(782/824). From these two groups 49 differential protein spots were identified, of which over 3 times the difference in the expression of 30 protein spots were singled out and MALDI-TOF-MS analysis was carried out. Ten proteins were identified. Upregulated expression was observed in alpha-2-macroglobulin, B-cell receptor-associated protein, keratin 1,apolipoprotein A-I, and down-regulated expression was observed in haptoglobin, α2-heremans-schimid-glycoprotein,mitogen-activated protein kinase 4, zinc finger protein 323, ZAP-70 and SP40 in the patient group. Conclusions The well-resolved and reproducible 2-DE serum patterns of patients are established and some differentially expressed proteins are characterized. Whether these proteins of differential expression are serum markers for liver injury resulting from coal-burning type of arsenism need to be further verified.

OBJECTIVETo explore the effect of Bushen Huoxue Compound (BHC) on lactate dehydrogenase (LDH) leakage, expressions of vascular endothelial growth factor (VEGF) and VEGF mRNA in retinal Muller cells under high glucose condition or advanced glycosylation end products (AGEs) condition by using serum pharmacological method.

METHODSThe retinal Müller cells of 5-7 days post-natal Sprague Dawley (SD) rats were cultured with modified enzyme-digestion method. Purified retinal Muller cells were cultured in normal conditions, high glucose condition (50 mmol/L) or AGEs (50 mg/L and 100 mg/L) conditions, and BHC-containing serum was added to culture medium. The LDH leakage and VEGF expressions were measured by enzyme-linked immunosorbent assay (ELISA). In addition, the relative expression of VEGF mRNA was tested by reverse transcription polymerase chain reaction (RT-PCR).

RESULTSCompared with the normal control group, expressions of VEGF and VEGF mRNA were significantly increased in the high glucose group, the low dose AGEs group and the high dose AGEs group (all P < 0.01). The LDH leakage was obviously increased in the high dose AGEs group, when compared with the normal control group and the high glucose group (P < 0.01). The LDH leakage, expressions of VEGF and VEGF mRNA were obviously decreased by BHC-containing serum both in high glucose and AGEs conditions (P < 0.05, P < 0.01). BHC-containing serum had no significant effect on the LDH leakage and expressions of VEGF and VEGF mRNA in normal conditions (P > 0.05).

CONCLUSIONSAGEs intervention could obviously lower the stability of Müller cell membrane. Up-regulated expressions of VEGF and VEGF mRNA in cultured Müller cells could be induced by AGEs or high glucose. BHC-containing serum could stabilize the stability of Müller cell membrane, inhibit the transcription of VEGF mRNA and decrease the protein expression of VEGF, which might be one of important mechanisms for preventing and treating diabetic retinopathy.

Animals ; Cells, Cultured ; Diabetic Retinopathy ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Ependymoglial Cells ; Glucose ; L-Lactate Dehydrogenase ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A

To promote bilingual teaching reform and explore a proper bilingual teaching mode in China,we studied the bilingual teaching of the course “Biochemistry on special subjects”.The present paper mainly designs and discusses the object of the course,teaching materials,contents and methods as well as the building of feedback and evaluation system of the course.

OBJECTIVETo explore the protective effect and the mechanism of Puerarin Injection (PI) on myocardial ischemia reperfusion in patients with coronary heart disease (CHD) and angina pectoris (AP).

METHODSSeventy-eight patients with AP planned to receive the PTCA and stenting treatment were randomly divided and single-blindedly into the conventional group and the PI group. Based on the conventional treatment and pre-operational preparation, the PI group was given 200 ml of PI by intravenous dripping once a day, beginning from one week before operation, but to the conventional group, normal saline was given for instead. The condition of AP attack in balloon dilatatory stage of PTCA was observed and change of ST segment of ECG detected by a 12-lead ECG monitor. The blood levels of von Willebrand factor (vWF:Ag), nitric oxide (NO) and endothelin-1 (ET-1) were also observed before and after treatment.

RESULTSAs compared with those in the conventional group, number of patients having AP attack and ST segment change in PTCA process was lessened in the PI group, with blood levels of vWF:Ag and ET-1 obviously lower, and NO content obviously higher than those in the conventional group,

CONCLUSIONSPI could protect the myocardium in 2-3 days after ischemia reperfusion, one of the possible reasons is that PI can simulate the late phase of ischemic preconditioning, which may be related to its effect in lowering plasma vWF:Ag and ET-1, and increasing the serum NO content.

Angina Pectoris ; therapy ; Angioplasty, Balloon, Coronary ; Antigens ; blood ; Endothelin-1 ; blood ; Female ; Humans ; Infusions, Intravenous ; Isoflavones ; therapeutic use ; Male ; Middle Aged ; Myocardial Reperfusion Injury ; prevention & control ; Nitric Oxide ; blood ; Stents ; von Willebrand Factor ; immunology

The present study was designed to observe the expressions of bone morphogenetic protein-7 (BMP-7) and inhibitory Smads in kidney of rats with diabetic nephropathy (DN), and explore the possible mechanism of DN. Male Wistar rats weighing 180-220 g were single injected with streptozocin (STZ, 55 mg/kg body weight) for 2, 4, 8 and 16 weeks to induce DN. Blood glucose, kidney weight/body weight and 24-hour urine protein in the control and DN rats were examined; the expressions of BMP-7, Smad6 and Smad7 were detected by using immunohistochemical techniques, Western blot and real-time PCR. The results showed that blood glucose and 24-hour urine protein in DN rats were higher than that in the control rats and kidney weight/body weight was also elevated in DN rats, especially in 16-week STZ-induced rats. The expressions of BMP-7 and Smad6 proteins in DN rats were elevated, while BMP-7 mRNA expression was increased 2 weeks after STZ injection and decreased 16 weeks after STZ injection. The expressions of Smad7 protein and mRNA were elevated in DN rats 2 weeks after STZ injection and decreased 16 weeks after STZ injection. In addition, the expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I (COL-I) mRNA were increased in DN rats. These results suggest in the early stage of DN, increase in BMP-7 and inhibitory Smad expression may play a role in the feedback regulation and restrain the development of DN.
Animals ; Bone Morphogenetic Protein 7 ; genetics ; metabolism ; Collagen Type I ; metabolism ; Diabetes Mellitus, Experimental ; metabolism ; Diabetic Nephropathies ; metabolism ; Kidney ; metabolism ; pathology ; Male ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Smad6 Protein ; genetics ; metabolism ; Smad7 Protein ; genetics ; metabolism ; Transforming Growth Factor beta1 ; metabolism