Objective: To investigate the effect of vitamin B12 on the growth and hemopoiesis of broilers. Methods: The Arbor Acres broilers were fed the experimental diets with different doses of vitamin B12 0.00, 0.008, 0.016, 0.024 mg/kg for 3 weeks. The body weight gain and hematologic indices of the broilers were measured. Results: Vitamin B12 deficiency in the diet could depress the body weight gain and feed conversion ratio of the broilers, decrease the amount of red blood cell and hemoglobin, enlarge the volume of red blood cell, increase the content of each cell hemoglobin, reduce platelet in blood. While 0.008 mg/kg vitamin B12 was added in the experimental diets, the body weight gain and feed conversion ratio of the broilers increased markedly. Furthermore, when 0.016mg/kg vitamin B12 was added to the diet, the number of the red blood cell and the content of hemoglobin of the broilers increased significantly, and the shape and volume of the red blood cell became ordinary. There were significants interrelations between BWG,RBC,Hb,PCV,PLT,MCV,MCH of the broilers and the addition of vitamin B12 in the diet. Conclusion: Vitamin B12 deficiency could result in the megaloblastic animia. 0.02-0.03 mg vitamin B12 per kilo diet was required to maintain the growth and normal hemopoiesis of the broilers.

AIM: To explore the roles of heat shock protein 90 (HSP90) in the blockage of hydrogen sulfide (H2S) against chemical hypoxia-mimetic agent (cobalt chloride, CoCl_2)-induced oxidative stress injuries in H9c2 cardiac cell. METHODS: H9c2 cells were treated with CoCl_2 to set up the chemical hypoxia-induced the model of cardiomyocyte injury. Sodium hydrosulfide (NaHS, a H2S donor) was added into medium for 30 min before CoCl_2 treatment. ATP content was detected by high performance liquid chromatogram (HPLC). Mitochondrial membrane potential (MMP) was measured by rhodamine123 (Rh123) staining and photofluorography. The activity of superoxide dismutase (SOD) was observed using a SOD kit. The expression of heme oxygenase-1 (HO-1) was evaluated by Western blotting. RESULTS: CoCl_2 at concentration of 600 μmol/L significantly reduced SOD activity, ATP level and MMP, and enhanced the expression of HO-1 in H9c2 cells. Pretreatment with 400 μmol/L NaHS dramatically inhibited the cytotoxicity induced by CoCl_2, increased SOD activity, ATP level and MMP, decreased HO-1 expression. 17-allylamino-17 demethoxygeldanamycine(17AAG), an inhibitor of HSP90, obviously blocked the inhibitory effect of H2S on the CoCl_2-induced cytotoxicity, reduced the levels of ATP and MMP, increased HO-1 expression. However, no significantly influence on SOD activity was observed. CONCLUSION: HSP90 may mediate the cardioprotection of H2S via inhibiting the oxidative stress induced by chemical hypoxia.