大鼠成体心肌细胞的分离和培养

目的: 探索稳定的大鼠成体心肌细胞的分离和培养方法. 方法: 应用主动脉逆行生物酶(5 g/L胰蛋白酶及1 g/L胶原酶)灌流法分离大鼠成体心肌细胞,免疫荧光染色法鉴定分离的心肌细胞,比较有无血清培养对心肌细胞的影响. 结果: 心肌细胞的存活率为95%以上;存活细胞呈杆状,形态完整,长宽比约为4～6∶ 1;无血清培养心肌细胞只能存活1 wk,形态不发生改变;而加血清培养心肌细胞可存活2 wk以上,但超微结构发生了改变,且不同血清浓度对成纤维细胞生长具有不同的作用. 结论: 主动脉逆行生物酶(胶原酶和蛋白酶)灌流法是比较理想的心肌细胞分离方法;血清对成体心肌细胞的培养起着重要作用.     

Effects of AT1 receptor antagonist, losartan, on rat hepatic fibrosis induced by CCl(4)

AIM:To investigate effect of losartan, an AT1 receptor antagonist, on hepatic fibrosis induced by CCl(4); and to determine whether or not AT1 receptors are expressed on hepatic stellate cells. METHODS AND RESULTS:Fifty male Sprague-Dawley rats, weighing (180 plus minus20)g, were randomized into five groups (control group, model group, and three losartan treated groups), in which all rats were given the subcutaneous injection of 40% CCl(4)(every 3 days for 6 weeks) except for rats of control group. Rats of losartan-treated groups were treated with losartan (20 mg/kg, 10 mg/kg, 5 mg/kg, daily gavage). After 6 weeks liver tissue and serum samples of all rats were examined. Serum hyaluronic acid (HA), procollagen type III (PC III) were detected by radioimmunoassays. van Giesion collagen staining was used to evaluate the extracellular matrix of rats with liver fibrosis. The expression of AT1 receptors, transforming growth factor-beta (TGF-beta), and alpha-smooth muscle actinalpha-SMA) in liver tissue were determined by immunohistochemical techniques. Compared with model group, serum ALT and AST of losartan-treated groups were significantly reduced (italic>t = 4.20,P < 0.01 and italic>t = 4.57,P < 0.01). Serum HA and PC III also had significant differences (italic>t = 3.53,P<0.01 and t=2.20, P<0.05). The degree of fibrosis was improved by losartan and correlated with the expressions of AT1 receptors, TGF-beta, and alpha-SMA in liver tissue.CONCLUSION:AT1 receptor antagonist, losartan, could limit the progression of the hepatic fibrosis induced by CCl(4). The mechanism may be related to the decrease in the expression of AT1 receptors and TGF-beta, ameliorating the injury of hepatocytes; activation of local renin-angiotensin system might relate to hepatic fibrosis; and during progression of fibrosis, activated hepatic stellate cells might express AT1 receptors.     

Associations of self-esteem,dysfunctional beliefs and coping style with depression in patients with schizophrenia: A preliminary survey

Psychological models of depression in schizophrenia have proposed that cognitive structures (e.g., self-esteem, dysfunctional beliefs) may have a role in the development and maintenance of depression. However, it has not been clear what the characteristics of these cognitive structures were in people with schizophrenia and whether they have an independent association with depression, especially in those from a Chinese cultural background. The present investigation examined 133 people with schizophrenia and 50 healthy controls and indicated that compared to the controls people with schizophrenia showed lower self-esteem, higher levels of dysfunctional beliefs and negative coping styles. Multiple linear regression analysis revealed that only low frustration tolerance, problem solving and self-blame were found to be the independent correlates of depression in schizophrenia. Results are discussed with the view of clinical implications of cognitive formulation and therapy for schizophrenia in China.     

Suicide attempt and suicidal ideation and their associations with demographic and clinical correlates and quality of life in Chinese schizophrenia patients

Objectives

This study aimed to examine the prevalence and correlates of lifetime suicide attempts and current suicidal ideation in community-dwelling schizophrenia patients in China.

Method

A sample of 540 schizophrenia patients was randomly selected in Beijing, China. All subjects were interviewed using standardized assessment instruments and their basic socio-demographic and clinical data including history of suicide attempts were collected.

Results

The prevalence of lifetime suicide attempts and the point prevalence of suicidal ideation were 12.0 %, and 21.1 %, respectively. In multiple logistic regression analyses, the presence of lifetime suicide attempt was independently associated with rural residence, having major medical conditions and better social functioning, while higher likelihood of current suicidal ideation was associated with past suicide attempt, the severity of overall psychopathology and depressive symptoms and lower psychological quality of life (QOL).

Conclusion

Among Chinese outpatients with schizophrenia, increased current symptoms and poorer QOL were correlated with current suicidal ideation, while demographic factors and indicators of greater social support were mostly correlated with lifetime suicide attempts. This study may help to identify important subgroups of patients with schizophrenia at particularly high risk of suicidal behavior.     

Anti-Inflammatory Effects of Apigenin in Lipopolysaccharide-Induced Inflammatory in Acute Lung Injury by Suppressing COX-2 and NF-kB Pathway

This study aims to evaluate the possible mechanisms responsible for the anti-inflammatory effects of apigenin lipopolysaccharide (LPS)-induced inflammatory in acute lung injury. In this study, the anti-inflammatory effects of apigenin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the possible mechanisms involved in this protection were investigated. Pretreatment with apigenin prior to the administration of intratracheal LPS significantly induced a decrease in lung wet weight/dry weight ratio in total leukocyte number and neutrophil percent in the bronchoalveolar lavage fluid (BALF) and in IL-6 and IL-1β, the tumor neurosis factor-α (TNF-α) in the BALF. These results showed that anti-inflammatory effects of apigenin against the LPS-induced ALI may be due to its ability of primary inhibition of cyclooxygenase-2 (COX-2) gene expression and nuclear factor kB (NF-kB) gene expression of lung. The results presented here suggest that the protective mechanism of apigenin may be attributed partly to decreased production of proinflammatory cytokines through the inhibition of COX-2 and NF-kB activation. The results support that use of apigenin is beneficial in the treatment of ALI.