ABSTRACT
Objective To quantitatively assess the myocardial triglyceride (TG) content in type 2 diabetes mellitus (T2DM) patients with non-alcoholic fatty liver disease (NAFLD) using 1H-magnetic resonance spectroscopy (1H-MRS), and to explore the correlation of TG content with cardiac function parameters and serum biochemical indexes. Methods Fifty-two T2DM patients diagnosed from Jan. 2017 to Aug. 2018 were enrolled. Serum biochemical parameters were measured, and left ventricular function and myocardial relative TG content were evaluated by 1H-MRS. Dixon technique was used to perform abdominal magnetic resonance imaging to evaluate the percentage of liver lipid content. Pearson correlation analysis was used to investigate the correlation between myocardial relative TG content and cardiac function parameters and serum biochemical indicators. Results The abdominal Dixon technique showed that the percentage of liver lipid content of the T2DM patients with NAFLD was higher than that of the patients without NAFLD ([14.99±5.21]% vs [3.51±1.75]%), and the difference was significant (t= -7.209, P<0.01). 1H-MRS showed that the myocardial relative TG content was higher in the T2DM patients with NAFLD than that in the patients without NAFLD ([1.87±0.55]% vs [1.19±0.48]%), and the difference was significant (t=-4.105, P<0.01). The myocardial relative TG content of the T2DM patients was significantly positively correlated to the percentage of liver lipid content, interventricular septal thickness (IVS), fasting blood-glucose and left ventricular mass to end-diastolic volume ratio (LVMVR; r= 0.582, 0.293, 0.318, and 0.282; P=0.001, 0.035, 0.021, and 0.042). Conclusion 1H-MRS is a non-invasive quantitative evaluation method for the abnormal metabolism of myocardial TG in the T2DM patients with NAFLD. The myocardial relative TG content of the T2DM patients with NAFLD is related to the percentage of liver lipid content, IVS, fasting blood glucose and LVMVR.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the apoptosis-inducing effects of emodin on multidrug resistant leukemia cell line K562/Adr, and to explore the role of Akt-Caspase 3 signal pathway in apoptosis of K562/Adr cells treated with emodin.</p><p><b>METHODS</b>K562/Adr cells were exposed to emodin of different doses. The ability of emodin to induce apoptosis of K562/Adr cells was detected by Annexin V/PI double labeled flow cytometry and DNA ploidy analysis, the expressions of procaspase-3, PARP, Akt, p-Akt protein were determined by Western blot.</p><p><b>RESULTS</b>Apoptosis in K562/Adr cells could be induced by emodin in a dose dependent manner, Western blot results showed that emodin down-regulated the expression levels of procaspase-3, Akt, p-Akt, PARA 116 KD in treated K562/Adr cells, up-regulated expressions leves of PARP 85 KD in a time-dependent manner.</p><p><b>CONCLUSION</b>The Akt-Caspase 3 signal pathway may be involved in these processes.</p>