Protective effects of Sapindus saponins in spontaneously hypertensive rats / 中国结合医学杂志

<p><b>OBJECTIVES</b>To investigate the protective effects of Sapindus saponins in spontaneously hypertensive rats, and the possible cellular and molecular mechanisms.</p><p><b>METHODS</b>Thirty-two 16-week-old spontaneously hypertensive rats were randomly divided into four groups (8 in each group): model group (placebo), positive control group (27 mg/kg of Captopril Tablets), Sapindus saponins groups (27 mg/kg and 108 mg/kg, respectively). Another 8 healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for 8 weeks. Blood pressure of rats was determined by non-invasive blood pressure meter (BP-6). Furthermore, the contents of angiotensin II (Ang II) in plasma and myocardial tissue were determined by enzyme-linked immunosorbent assay (ELISA), the gene expression of receptor angiotensin type 1 (AT1R) in aorta was determined by quantitative realtime polymerase chain reaction (qRT-PCR). The protein expression of transforming growth factor-β1 (TGF-β1) and AT1R in heart was determined by immunohistochemical staining. The protein expression of p-phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK) was determined by Western blotting. The contents of interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF) in serum were determined by radioimmunoassay. And the histopathological and morphological changes of aorta and heart tissue samples were assessed semi-quantitatively by hematoxylin-eosin (HE) or Masson staining.</p><p><b>RESULTS</b>Thirty minutes after single or continuous treatment, systolic blood pressure (SBP) was reduced significantly in Sapindus saponins groups. And the contents of AngII, IL-1, IL-6 and TNF-α in serum, the expression of AT1R mRNA, p-p38MAPK and TGF-β1 were significantly suppressed dose-dependently (P<0.05 or P<0.01). With the Sapindus saponins treatment, compared with those of the model group, the cardiac and aortic pathological changes were ameliorated significantly.</p><p><b>CONCLUSIONS</b>Our findings suggest that Sapindus saponins might have protective effects in spontaneously hypertensive rats, the cellular and molecular mechanisms of which might be relevant to the regulation of inflammatory responses mediated by p-p38MAPK signal pathway based on activated Ang II and AT1R.</p>

Equity of health service utilization of urban residents: data from a western Chinese city / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Getting medical treatment is still difficult and expensive in western China. Improving the equity of basic health services is one of the tasks of the new healthcare reform in China. This study aimed to analyze the parallel and vertical equity of health service utilization of urban residents and then find its influencing factors.</p><p><b>METHODS</b>In August 2011, a household survey was conducted at 18 communities of Baoji City by multi-stage stratified random sampling. Based on the survey data, we calculated a concentration index of health service utilization for different income residents and a difference index of different ages. We then investigated the influencing factors of health service utilization by employing the Logistic regression model and log-linear regression model.</p><p><b>RESULTS</b>The two-week morbidity rate of sampled residents was 19.43%, the morbidity rate of chronic diseases was 21.68%, and the required hospitalization rate after medical diagnosis was 11.36%. Among out-patient service utilization, the two-week out-patient rate, number of two-week out-patients, and out-patient expense had good parallel and vertical equity, while out-patient compensation expense had poor parallel and vertical equity. The inpatient service utilization, hospitalization rate, number of inpatients, days stayed in the hospital, and inpatient expense had good parallel equity, while inpatient compensation expense had poor parallel equity. While the hospitalization rate and number of inpatients had vertical equity, the days stayed in hospital, inpatient expense, and inpatient compensation expense had vertical inequity.</p><p><b>CONCLUSIONS</b>Urban residents' health was at a low level and there was not good health service utilization. There existed rather poor equity of out-patient compensation expense. The equity of inpatient service utilization was quite poor. Income difference and the type of medical insurance had great effects on the equity of health service utilization.</p>

Effects of sapindus saponins on inflammatory response mediated by Ang II/p38MAPK pathway and cardiac hypertrophy in spontaneously hypertensive rats / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the effects of sapindus saponins on myocardial inflammation mediated by Ang II/ p38MAPK signal pathway and cardiac hypertrophy in spontaneously hypertensive rats. And also to explore the correlation of cardiac hypertrophy and inflammation.</p><p><b>METHOD</b>Thirty-two 16-week-old spontaneously hypertensive rats (SHR) were randomly divided into four groups, one with placebo as model group, one with captopril tablets (27 mg x kg(-1)) as positive control, one with low-dose sapindus saponins (27 mg x kg(-1)), one with high-dose (108 mg x kg(-1)). And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the indicators detected were as follows: (1) left ventricular mass index (LVMI); (2) the content of Ang II and hs-CRP in plasma were determined by ELISA; (3) the protein expression of AT1R and VEGF were determined by immunohistochemical method; (4) the protein expression of p-p38MAPK in myocardial cells was determined by Western blot.</p><p><b>RESULT</b>Sapindus saponins reduced LVMI, and blocked the expression level of Ang II, AT1R, p-p38MAPK, VEGF and hs-CRP in myocardial tissue. Vs the SHR model group, there were significant differences (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Our findings suggested that sapindus saponins could inhibited cardiac hypertrophy, the possible mechanisms may be related to the inhibition on inflammatory response mediated by Ang II/p38MAPK pathway.</p>