Effect of meal replacements on body weight control and blood glucose and lipid profile / 中华内分泌代谢杂志

Objective To assess the effect of meal replacements on body weight control and blood glucose and lipid profile by adjusting their nutrients intake with a meal replacement approach.Methods One hundred and thirty subjects were randomly divided into intervention group (100 subjects) and control group (30 subjects).Besides dietary consulting and health education,all subjects in intervention group received a dietary treatment with 2 meal replacements each day over a shot-term (3 months).All subjects were evaluated by recording the body measurements and laboratory data every 2 weeks.Results Compared with the baseline,mean percentages of BMI loss and decrease in waist circumference were 7.2 ％ and 6.5％ for intervention group(P＜0.01) by week 12.Meanwhile,systolic blood pressure,diastolic blood pressure,fasting plasma glucose,and triglyceride levels were significantly reduced (P＜0.01),showing significant difference compared with control group at the same period(all P＜0.01).Conclusion The meal replacement approach evaluated is an effective strategy to control body weight,and thus to achieve great improvement in the prevention of obesity-related diseases.

Protective effects of luteolin on neurons against oxygen-glucose deprivation/reperfusion injury via improving Na+/K+ -ATPase activity / 中国中药杂志

<p><b>OBJECTIVE</b>Luteolin, a flavone, has considerable neuroprotective effects by its anti-oxidative mechanism. However, it is still unclear whether luteolin can protect neurons against oxygen-glucose deprivation/reperfusion (OGD/R) induced injury.</p><p><b>METHOD</b>After 2 hours oxygen-glucose deprivation and 24 hours reperfusion treatment in primary cultured hippocampal neurons, the neuron viability, survival rate and apoptosis rate were evaluated by MTT assay, lactate dehydrogenase (LDH) leakage assay and Hoechst staining, respectively. The activity of Na+/K+ -ATPase was examined in cultured neurons or in the hippocampus of SD rats treated by 10 minutes global cerebral ischemia and followed 24 hours reperfusion.</p><p><b>RESULT</b>Treatment by OGD/R markedly reduced neuronal viability, increased LDH leakage rate and increased apoptosis rate. Application of luteolin (10-100 micromol x L(-1)) during OGD inhibited OGD/R induced neuron injury and apoptosis in a dose-dependent manner. Compared to the control group or OGP/R-treated neurons, the activity of Na+/K+ -ATPase was significantly suppressed in global ischemia/reperfusion group or OGD/R-treated neurons. Application of luteolin during ischemia or OGD preserved the Na+/K+ -ATPase activity. Furthermore, inhibition of Na+/K+ -ATPase with ouabain attenuated the protective effect afforded by luteolin.</p><p><b>CONCLUSION</b>The data provide the evidence that luteolin has neuroprotective effect against OGD/R induced injury and the protective effect may be associated with its ability to improve Na+/K+ -ATPase activity after OGD/R.</p>

The disturbance of calcium metabolism of vascular smooth muscle in the late phase of septic shock and the underlying mechanism / 中国病理生理杂志

AIM: To evaluate the alterations in calcium metabolism of the vascular smooth muscle in the late phase of septic shock and test the hypothesis that nitric oxide might be involved in sepsis-induced vascular hyporeactivity. METHODS: Male Sprague-Dawley rats were subjected to sepsis by cecal ligation and puncture (CLP). 18 hours post CLP,rat aortic rings were employed for measurement of contractile responses by using organ bath technique. RESULTS: In endothelium-denuded aortic rings from CLP rats,concentration-contraction curves to phenylephrine (PE) and KCl were significantly decreased when compared to that from sham control rats. The transient contraction induced by PE in calcium-free Krebs solution and the concentration-dependent contraction to CaCl_2 in KCl-depolarized medium were also markedly reduced. The hyporeactivity was partially reversed by treatment with aminoguanidine,a selective inducible nitric oxide synthase inhibitor. CONCLUSION: An impairment in calcium handling in vascular smooth muscle is involved in the vascular hyporeactivity during the late phase of septic shock,in which an excessive nitric oxide production might be the major mechanism.