Polymorphisms of the myostatin gene and its relationship with reproduction traits in the Bian chicken.

Myostatin, or growth and differentiation factor 8, is a member of the transforming growth factor-ß superfamily; it functions as a negative regulator of skeletal muscle development and growth in mammals. In this study, single nucleotide polymorphisms in the 5' regulatory region and exon 1 of the myostatin gene were detected by PCR-SSCP in the Bian, Jinghai, Youxi, and Arbor Acre chickens, and the associations of the polymorphisms with reproduction traits were analyzed. Seven SNPs (A326G, C334G, C1346T, G1375A, A1473G, G1491A, and G2283A) were found in the myostatin gene. Association analysis showed that the G2283A were significantly associated with reproduction traits. Bian chickens of the GG genotype had a greater age at first egg than those of the GA and AA genotypes (P<0.01). Correspondingly, Bian chickens of the GA and AA genotypes had larger egg number at 300 days than those of the GG genotype (P<0.05 and P<0.01, respectively). Bian chickens of the AA genotype had significantly higher body weight at 300 days than those of the GG genotype (P<0.05). These results suggested that the myostatin gene may have certain effects on reproduction traits other than merely as a negative regulator of skeletal muscle development and growth in mammals previously reported.

Polymorphism in exons of the myostatin gene and its relationship with body weight traits in the Bian chicken.

In our research, single nucleotide polymorphisms (SNPs) of exon regions of the myostatin gene were detected by PCR-SSCP in the Bian chicken and three reference chicken populations (Jinghai, Youxi, and Arbor Acre). Four novel SNPs (G2283A, C7552T, C7638T, and T7661A) were detected. The findings from the least square means showed that Bian chickens with EE and DE genotypes had significantly higher body weight, at 6-18 weeks of age, than those of the DD genotype (P < 0.05). The results suggest that the mutation G2283A, detected in exon 1, has potential as a genetic marker for body weight traits in the Bian chicken.

[Protective effect of ischemia postconditioning on reperfusion injury in patients with ST-segment elevation acute myocardial infarction].

OBJECTIVE: To observe the effect of ischemia postconditioning during the first minutes of reperfusion for the myocardial reperfusion injury in ST-segment elevation acute myocardial infarction (STEMI) patients undergoing emergency percutaneous coronary intervention (PCI). METHODS: STEMI patients undergoing emergency PCI in affiliated hospital of Beihua University between October 2006 and January 2009 were randomly divided into two groups: the control group (n = 34) without any intervention after PTCA, and the postconditioning group (n = 30) with ischemia postconditioning within first minutes of reflow by 3 episodes of 30-second inflation and 30-second deflation with the angioplasty balloon. Reperfusion arrhythmias, CK and CKMB, corrected TIMI frame count (CTFC), wall motion score index (WMSI) and left ventricular ejection fraction (LVEF) by echocardiography were compared between the two groups. MI areas were evaluated with the ECG-54 criteria/32 system and myocardial blush grade (MBG) was measured. RESULTS: The incidence of reperfusion arrhythmias-frequent ventricular premature (26.7% vs. 52.9%) and short array ventricular tachycardia beat (23.3% vs. 58.8%) as well as values of peaks CK [(1162 ± 548) U/L vs. (1732 ± 480) U/L, P < 0.01], CKMB [(165 ± 70) U/L vs. (280 ± 99) U/L, P < 0.01], CTFC (22.23 ± 3.81 vs. 26.97 ± 3.42), WMSI (1.27 ± 0.52 vs. 1.82 ± 0.83), and infarction areas determined by ECG methods (10.60% ± 4.97% vs.14.65% ± 6.88%, all P < 0.05) were all significantly lower in the postconditioning group than in control group while LVEF (0.55 ± 0.08 vs. 0.47 ± 0.10) and MBG (2.27 ± 0.64 vs. 1.47 ± 0.61, all P < 0.05) were significantly higher in the postconditioning group than in control group. CONCLUSIONS: Ischemia postconditioning can significantly reduce myocardial reperfusion injury in patients with STEMI.

Neuroprotective effect of matrine on MPTP-induced Parkinson's disease and on Nrf2 expression.

The incidence rate of Parkinson's disease (PD) is ≤2% in Chinese individuals >65 years old, accounting for 40% of the global total of PD patients. The pathogenesis of PD is not yet clear, and oxidative stress-induced mitochondrial dysfunction is considered to be the main reason for the onset of PD. Studies have shown that matrine exhibits good antioxidant activity. Thus, the present study aimed to observe the protective effect and mechanism of matrine on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neuron damage. A total of 25 C57BL male mice were randomly divided into 5 groups, consisting of the control group (group A), the MPTP group (group B) and three matrine (4, 8 and 16 mg/kg) plus MPTP treatment groups (groups C, D and E, respectively). Results from a pole-climbing test and locomotor activity experiments were recorded. The mice were sacrificed 4 days later and brain dissection was performed. The levels of superoxide dismutase (SOD) and glutathione (GSH) were assessed. The expression level of tyrosine hydroxylase (TH) in the ventral midbrain was studied by immunofluorescence analysis. The expression level of nuclear factor erythroid 2-related factor 2 (Nrf2) in the ventral midbrain was studied by western blot analysis. The experiments were repeated three times. Compared with control mice, the PD mice exhibited the typical behaviors associated with PD; matrine can alleviate this phenomenon, and with increasing matrine concentration, the symptoms were reduced significantly. Compared with the control mice, the PD mice had lower SOD and GSH activity, and matrine partially reversed the change in SOD and GSH activity. Immunofluorescence analysis showed that the level of TH in the ventral midbrain decreased significantly in the PD mice, and that the mice administered matrine showed higher expression of TH and levels of TH-positive cells. Western blotting results showed that the expression of Nrf2 in the ventral midbrain decreased significantly in the PD mice, and that matrine was able to reverse this phenomenon. In conclusion, by promoting antioxidant-related Nrf2 signaling pathways in the ventral midbrain, matrine can inhibit the oxidative damage of dopamine neurons in PD.

Treatment with PPARα Agonist Clofibrate Inhibits the Transcription and Activation of SREBPs and Reduces Triglyceride and Cholesterol Levels in Liver of Broiler Chickens.

PPARα agonist clofibrate reduces cholesterol and fatty acid concentrations in rodent liver by an inhibition of SREBP-dependent gene expression. In present study we investigated the regulation mechanisms of the triglyceride- and cholesterol-lowering effect of the PPARα agonist clofibrate in broiler chickens. We observed that PPARα agonist clofibrate decreases the mRNA and protein levels of LXRα and the mRNA and both precursor and nuclear protein levels of SREBP1 and SREBP2 as well as the mRNA levels of the SREBP1 (FASN and GPAM) and SREBP2 (HMGCR and LDLR) target genes in the liver of treated broiler chickens compared to control group, whereas the mRNA level of INSIG2, which inhibits SREBP activation, was increased in the liver of treated broiler chickens compared to control group. Taken together, the effects of PPARα agonist clofibrate on lipid metabolism in liver of broiler chickens involve inhibiting transcription and activation of SREBPs and SREBP-dependent lipogenic and cholesterologenic gene expression, thereby resulting in a reduction of the triglyceride and cholesterol levels in liver of broiler chickens.

Protective effect of Schisandrae chinensis oil on pancreatic ß-cells in diabetic rats.

Islet cell dysfunction in type 2 diabetes is primarily attributed to increased apoptosis of pancreatic ß-Cells. The aim of the present study was to investigate the effects of Schisandrae chinensis oil on pancreatic ß-Cells in type 2 diabetes mellitus rats and the associated molecular mechanisms of action. Wistar rats were randomly divided into diabetic rats and control rats, diabetic rats treated with Schisandrae chinensis oil (1 mg/kg), and control rats treated with Schisandrae chinensis oil. The serum fasting blood glucose, insulin, total cholesterol, and triglyceride levels along with MDA content, SOD and CAT activities in pancreatic tissues were measured. TUNEL was used to observe the apoptosis of rat pancreatic cells. Western blot was used to determine specific protein expression. The results showed that the oil significantly decreased fasting blood glucose, total cholesterol, triglyceride levels as well as the pancreatic MDA, but increased SOD and CAT activities. The protein expression of Bcl-2, PDX-1, GLUT-2, and GCK but not caspase 3 was significantly enhanced in the oil-treated rats compared with diabetic rats. However, Bax content was not significantly different between the control and DM groups. Schisandra chinensis oil improves pancreatic ß-cell function by enhancing antioxidant potential of the pancreas, upregulating the expression of anti-apoptotic genes, increasing expression of glucose metabolism, and delaying islet cell apoptosis.