AIM:To study the effect of acyl coenzyme A:cholesteryl acyltransferase 1(ACAT1)antisense oligonucleotides on the formation of foam cells(FC).METHODS:THP-1 cells were cultured and differentiated into macrophages(MP)by phorbol myristate acetate(PMA).Over-expressing ACAT1 gene THP-1 cells were constructed.The ACAT1 antisense and missense oligonucleotides conducted by LipofectamineTM 2000 were incubated with above cells.Ac-LDL was added 6 h later and incubated for 24 h.The expression of ACAT1 protein was detected by Western blotting.The ACAT activity was measured by quantifying the incorporation of 1-14C oleoyl CoA into cholesteryl esters.The formation of foam cells was detected by oil red O staining.RESULTS:The ACAT1 antisense oligonucleotides inhibited the activity of ACAT in macrophages and over-expressing ACAT1 gene THP-1 cells.It also inhibited the formation of foam cell in macrophages and over-expressing ACAT1 gene THP-1 cells with lipid loading.The missense oligonucleotides did not show the inhibitory effects.CONCLUSION:The ACAT1 antisense oligonucleotides inhibit the activity of ACAT and the formation of foam cells.

Objective To explore the prognostic value of biomarkers in type 2 diabetic patients with acute myocardial infarction (AMI), this study was to investigate the associations between the neutrophil to lymphocyte ratio (NLR), the Global Registry of Acute Coronary Events (GRACE) score and in-hospital mortality. MethodsSeven hundred and seven consecutive AMI patients were divided into diabetic group (DM-AMI group), impaired glucose tolerance group (IGT-AMI group), and normal glycemic group (NGT-AMI group). The laboratory and clinical characteristics were assessed retrospectively from the medical records. The NLR and GRACE score were calculated. Results In AMI patients, the DM-AMI group had significantly higher NLR and GRACE scores compared with those from the IGT-AMI group and NGT-AMI group (P<0.01 or P<0.05). In DM-AMI group, the NLR and GRACE score were considerably elevated in the elderly DM-AMI group compared with their younger counterparts (both P<0.01). Furthermore, the NLR was considerably higher in the high-risk group than those in both the low- and medium-risk groups based on the GRACE score (both P<0.01). The NLR was positively correlated with the GRACE score in DM-AMI group(r=0.425, P<0.01). The NLR level and GRACE score were higher in the death group than those in surviving patients (both P<0.01). The optimal cut-off levels of 9.36 for NLR and 166 for GRACE score seem to predicte death in-hospital. Based on the receiver operating characteristic curve, when to predict death in-hospital, the best cutoff value of NLR was 9.36 (sensitivity 80.8%, specificity 69.6%; area under curve 0.787), and the best cutoff value of GRACE score was 166 (sensitivity 76.9%, specificity 76.4%; area under curve 0.778). Conclusion An elevated NLR is a potential predictor of in-hospital mortality in type 2 diabetic patients with AMI, which could help clinicians indentify high-risk patients and determine appropriate treatment strategies. <英文关鍵词>>=Neutrophil to lymphocyte ratio; In-hospital mortality; Acute myocardial infarction; Diabetes mellitus, type 2

The effect of atorvastatin on warfarin-induced aortic medial calcification and systolic blood pressure (SBP) of rats induced by warfarin was studied. Thirty healthy and adult rats were randomly divided into Warfarin group (n=10), Atorvastatin group (n=10) and normal control group (n=10). Caudal arterial pressure of rats was measured once a week, and 4 weeks later, aorta was obtained. Elastic fiber, collagen fiber and calcium accumulation in tunica media of cells were measured by Von Kossa staining. The results showed that warfarin treatment led to elevation of systolic blood pressure and aortic medial calcification. The chronic treatment also increased collagen, but decreased elastin in the aorta. However, the atorvastatin treatment had adverse effects. It was concluded that treatment with atorvastatin presented evidence of blood pressure lowing and calcification reducing. These data demonstrate that atorvastatin protected aortic media from warfarin-induced calcification and elevation of systolic blood pressure.
Aortic Diseases/chemically induced ; Aortic Diseases/drug therapy ; Aortic Diseases/*pathology ; Blood Pressure/*drug effects ; Calcinosis/chemically induced ; Calcinosis/*drug therapy ; Calcinosis/pathology ; Heptanoic Acids/*pharmacology ; Heptanoic Acids/therapeutic use ; Hypertension/chemically induced ; Hypertension/*drug therapy ; Pyrroles/*pharmacology ; Pyrroles/therapeutic use ; Random Allocation ; Rats, Wistar ; Warfarin

Summary: The effect of atorvastatin on warfarin-induced aortic medial calcification and systolic blood pressure (SBP) of rats induced by warfarin was studied. Thirty healthy and adult rats were randomly divided into Warfarin group (n=10), Atorvastatin group (n=10) and normal control group (n=10). Caudal arterial pressure of rats was measured once a week, and 4 weeks later, aorta was obtained. Elastic fiber, collagen fiber and calcium accumulation in tunica media of cells were measured by Von Kossa staining. The results showed that warfarin treatment led to elevation of systolic blood pressure and aortic medial calcification. The chronic treatment also increased collagen, but decreased elastin in the aorta. However, the atorvastatin treatment had adverse effects. It was concluded that treatment with atorvastatin presented evidence of blood pressure lowing and calcification reducing. These data demonstrate that atorvastatin protected aortic media from warfarin-induced calcification and elevation of systolic blood pressure.

Objective To observe the expression of autophagy-related genes and proteins in the smooth bladder muscle of rats after spinal cord injury (SPI).Methods Twenty-four male Wistar rats were randomly and evenly divided into a model group and a control group.The model group had SPI induced using the modified Allen's method,while the control group was only given laminectomy.Six hours after the operation,the Basso Beattle Bresnahan (BBB) locomotor rating scale was used to evaluate the rats' hindlimb locomotor function.Nissl staining was used to observe the morphological changes in their spinal cords,while Western blotting and immunofluorescence staining were employed to assess the expression of microtubule-associated protein 1 light chain 3 (LC3) and protein 62 (P62).The expression of autography gene Beclin1 mRNA was determined using a reverse transcription polymerase chain reaction (RT-PCR).Results The average BBB score in the model group was significantly lower than in the control group.After Nissl's staining,a decreased number of neurons and Nissl bodies was observed.Western blotting showed that the expression of LC3-Ⅱ had increased significantly and that of P62 had decreased significantly in the model group compared with the control group.The immunofluorescence staining showed LC3 and P62 dots in the bladders' smooth muscle cells.RT-PCR detected significantly higher LC3 and Beclinl mRNA levels in the model group than in the control group;in contrast the average P62 mRNA level was significantly lower.Conclusions Autophagy was activated in rats' bladder muscles after SPI.That may be related to the pathogenesis of a neurogenic bladder after spinal cord injury.