BACKGROUND: α-lipoic acid is named as “nature antioxidant” and “mitochondrial nutrition”. But it is unclear whether α-lipoic acid can be used to protect skeletal muscle with chronic hypoxia exposure, as wel as the relative mechanism. OBJECTIVE: To observe the effect of α-lipoic acid on the antioxidant enzymes and oxidative stress in rat skeletal muscle with chronic hypoxia exposure, and to investigate the relative signaling pathway of α-lipoic acid. METHODS: Thirty-six Sprague Dawley rats were randomly divided into three groups: normoxia control group, hypoxia control group, and hypoxia+α-lipoic acid group. Rats in the hypoxia control group were subjected to hypoxia exposure in normobaric hypoxic tent with 11.3% oxygen concentration. Rats in the hypoxia+α-lipoic acid group were induced by adding α-lipoic acid (0.25%) in the normal diet. Al the interventions were lasted for 4 weeks. RESULTS AND CONCLUSION: α-lipoic acid in hypoxia could markedly enhance the mitochondrial Sirtuin-3 expression, improve the mitochondrial adenosine triphosphate synthesis activity and membrane potential, up-regulate the mitochondrial state 3 respiratory rate, respiratory control ratio and ratio of phosphorus to oxygen, down-regulate the mitochondrial state 4 respiratory rate and promote and up-regulate the activity of mitochondrial antioxidant enzymes such as manganese superoxide dismutase, glutathione peroxidase and catalase, thus inhibiting mitochondrial H2O2 generation rate and reducing mitochondrial malondialdehyde level. The results indicated that α-lipoic acid could improve the efficiency of energy metabolism of chronic hypoxia skeletal muscle mitochondria and inhibit reactive oxygen generation, and it could inhibit the oxidative stress through improving antioxidant enzyme activity of mitochondria. The protection mechanism of α-lipoic acid on hypoxia skeletal muscle mitochondria may be related to the increasing of mitochondrial state 3 respiratory rate.

Adult ; Calcinosis ; Heart Aneurysm ; pathology ; Heart Ventricles ; Humans ; Male ; Thrombosis ; pathology

ObjectiveTo explore the diagnostic methods and surgery pattern at the first time of spontaneous perforation of congenital choledochal cyst.MethodsEleven cases(4 male,7 female) with spontaneous perforation of congenital choledochal cyst were 6 months to 5 years old,and their average course of disease were 4 days.Gustily abdominal distension,abdominal pain,crying and fever were present in all cases.Jaundice(7 cases) and emesis(5 cases) appeared.All cases were detected with physical sign of peritonitis by physical examination.Choledochal cysts were confirmed by CT or B ultrasound in 8 cases.All cases accepted abdominal paracentesis and biliary ascites was drawn.Three different operative procedures were performed:choledochocyst excision & Roux-Y choledocho-jejunostomy(2 cases),choledochotomy with T-tube drainage(3 cases),and cholecystostomy(6 cases).Nine children receiving external drainage operation accepted a second operation to rebuild biliary tract(choledochocyst excision & Roux-Y choledochoje-junostomy) after 3 to 6 months.ResultsAll cases had got satisfactory therapeutic efficacy without any grave complication such as fistula of anastomotic stoma,infection of biliary tract or obstruction of biliary tract.During operation,perforations were located in the juncture of choledochus and cystic duct in 5 children and were not found in the other 6 children.In the second operation,the cases receiving cholecystostomy had less peritoneal adhesion,anatomic structure changes,haemorrhage[(30-50) mL vs(100-200) mL] and operation time[(2.5-3.0) h vs(3.5-5.0) h] than those receiving choledochotomy with T-tube drainage,and did not appear inadequate drainage for cystic duct obstruction.ConclusionsFor children with more organ inflammatory edema and adherence and in a bad overall condition,the first-time operation of cholecystostomy is more reasonable.

Survivin is a protein that inhibits apoptosis and regulates cell division.The cDNA sequence of survivin was amplified by RT-PCR and sub-cloned into the prokaryotic expression vector pET-21b(+),followed by transformation into E.coli strain BL21(DE3) and induction with IPTG.The recombinant survivin protein fusing with 6?His tag was expressed in E.coli in the form of inclusion body at the expression level over 60% of the total cell protein.Results of Western blotting showed that recombinant survivin reacted specifically with anti-human survivin antibody.After gel filtration,the recombinant protein reached the purity over 95%,which facilitate the study of diagnosing and inhibitor agents targeting survivin.

To assess the effect of prostaglandin E_1(PGE_1)on renal blood flow and serum endothelin of liver recipients.Methods PGE_1 was administered in 38 liver recipients at the dose of 0.6?g?kg~(-1)?h~(-1)during liver transplantation and every day after operation.The effects of PGE_1 on serum endothelin concentration and creatinine(Cr)were observed and these indexes were compared with those in the control group(n=18).The renal blood flow resistance indexes(RI)were measured by Doppler ultrasound.Results Cr and RI were significantly lower in PGE1=treated group than those in the control group.PGE_1-treated group also showed a significantly lower serum endothelin concen- tration.Conclusion Administration of PGE_1 in liver recipients can significantly improve the early re- nal function by reducing serum endothelin concentration and dilating renal blood vessels.

The fruit of Pandanus tectorius (PTF) has a long history of use as a folk medicine to treat hyperlipidemia in Hainan province, South China. Our previous studies have shown that the n-butanol extract of PTF is rich in caffeoylquinic acids and has an adequate therapeutic effect on dyslipidemic animals induced by high-fat diet. In this work, seven caffeoylquinic acids isolated from PTF were screened for the lipid-lowering activity in HepG2 hepatoma cells. Oil-Red O staining, microscopy and intracellular triglyceride (TG) and total cholesterol (TC) quantification showed that 3-O-caffeoylquinic acid (3-CQA), 3, 5-di-O-caffeoylquinic acid (3,5-CQA), and 3,4,5-tri-O-caffeoylquinic acid (3,4,5-CQA) significantly inhibited lipid accumulation induced by oleic acid and decreased intracellular levels of TC and TG in a dose-dependent manner. These three caffeoylquinic acids showed no significant cytotoxicity at concentrations of 1 -50 μmol x L(-1) as determined by MTT assay. Realtime quantitative PCR revealed that 3-CQA and 3, 5-CQA significantly increased the expression of lipid oxidation-related genes PPARα, CPT-1 and ACOX1 while 3-CQA, 3, 5-CQA and 3,4,5-CQA decreased the expression of lipogenic genes SREBP-1c, SREBP-2, HMGR, ACC, FAS. Overall, 3-CQA, 3, 5-CQA and 3, 4, 5-CQA may be the principal hypolipidemic components in PTF which can decrease intracellular lipid accumulation through up-regulating the expression of lipid oxidative genes and down-regulating the expression of lipogenic genes.
Carcinoma, Hepatocellular ; metabolism ; China ; Cholesterol ; metabolism ; Gene Expression Regulation ; Hep G2 Cells ; Humans ; Lipid Metabolism ; Liver Neoplasms ; metabolism ; Oleic Acid ; Pandanaceae ; chemistry ; Quinic Acid ; analogs & derivatives ; chemistry ; Sterol Regulatory Element Binding Protein 1 ; Triglycerides ; metabolism

OBJECTIVETo observe the effect of β₃adrenoceptors (β₃-AR) activation on rat thoracic aorta smooth muscle contractility and the possible related mechanism.

METHODSThe endothelium removed thoracic aorta was pre-contracted with 30 mmol/L KCl physiological saline solution (PSS). Then the tension of the thoracic aorta was recorded in presence of BRL37344 (BRL) to determine the action of β₃-AR. The tension of the thoracic aorta was also recorded in the presence of Propranolol (PRA), SR59230A (SR), L-NNA, H-89 and Iberiotoxin (IBTX) respectively to reveal the underling mechanism of β₃-AR activation on rat vascular smooth muscle. Immunohistochemistry was adopted to confirm the existence and the distribution of β₃-AR in rat thoracic aorta.

RESULTSThe results showed that: (1) The thoracic aorta was relaxed by β₃-AR activation, with a relaxation percentage of (10.59 ± 0.79). (2) β₃-AR was expressed in both endothelial and smooth muscle layer in thoracic aorta sections of rats. (3) PRA did not block the effect of BRL on the thoracic aorta. The relaxation actions of BRL could be antagonized by pre-incubating the thoracic aorta with SR. (4) L-NNA (a NOS inhibitor) and H-89 (a PKA inhibitor) reversed the relaxation effect of BRL on vascular smooth muscle. (5) The effect of BRL was decreased after application of Ibriotoxin (IBTX), a large conductance calcium dependent potassium channel blocker.

CONCLUSIONThe results confirmed that activation of β₃-AR led to relaxation of thoracic aorta smooth muscle. The relaxation action of β₃-AR on smooth muscle of rat thoracic aorta was related to activation of NOS and PKA signaling pathway. Large conductance Ca²⁺-K⁺ channels were involved in the relaxation action of β₃-AR activation on rat thoracic aorta smooth muscle.

Animals ; Aorta, Thoracic ; physiology ; In Vitro Techniques ; Isoquinolines ; Large-Conductance Calcium-Activated Potassium Channels ; physiology ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular ; physiology ; Nitroarginine ; Peptides ; Propanolamines ; Propranolol ; Rats ; Receptors, Adrenergic, beta-3 ; physiology ; Signal Transduction ; Sulfonamides

OBJECTIVETo explore the effect of peimine on excision repair cross-complementation 1 (ERCC1) mRNA and lung resistant protein (LRP) expressions in A549/cisplatin (DDP) multidrug resistance (MDR) cell line.

METHODSLung cancer A549/DDP cells were cultured in vitro.Cells at logarithmic growth phase were divided into 4 groups, i.e., the blank control group, the DDP group, the ligustrazine group (DDP+ligustrazine), the peimine group (DDP + peimine). After 48-h drug action, ERCC1 mRNA expression was detected by RT-PCR and LRP expression detected by cell immunofluorescence.

RESULTSThere was no statistical difference in expression levels of ERCC1 mRNA and LRP between the DDP group and the blank control group (P > 0.05). Compared with the DDP group, expression levels of ERCC1 mRNA and LRP obviously decreased in the ligustrazine group and the peimine group (P < 0.05). They were obviously lower in the peimine group than in the ligustrazine group (P < 0.05).

CONCLUSIONSPeimine could reverse MDR of A549/DDP cell line. Its mechanism might be associated with down-regulating ERCC1 mRNA and LRP expression levels.

Cell Line, Tumor ; Cevanes ; pharmacology ; Cisplatin ; DNA-Binding Proteins ; genetics ; Down-Regulation ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; drug effects ; Endonucleases ; genetics ; Humans ; Low Density Lipoprotein Receptor-Related Protein-1 ; genetics ; Lung Neoplasms ; RNA, Messenger ; metabolism

Cerebral Infarction ; etiology ; Dextrocardia ; etiology ; Female ; Humans ; Infant ; Spleen ; abnormalities ; Syndrome

0.05).Conclusions The reduced expression of HLA-G on placenta in ICP patients may alter the maternal-fetal immune response and thus be involved in the pathogenesis of this disorder. Dexamethasone can upregulate the expression of HLA-G on placenta.The 14 bp deletion polymorphism in exon 8 of HLA-G gene might not have a significant influence on the development of ICP.