[Expression of steroidogenic enzymes in the rat model of polycystic ovary syndrome].

The aim of the present study was to investigate the expression changes of three steroidogenic enzymes in the polycystic ovary syndrome (PCOS). Thirty Sprague-Dawley (SD) rats were randomly divided into normal control (NC) group and PCOS group. PCOS rat model was established by DHEA injection. The serum levels of progesterone, estrogen and testosterone were measured by immunoradioassay or enzyme immunoassay. The cellular distributions of 3ß-hydroxy steroid dehydrogenase (3ß-HSD), 17ß-hydroxy steroid dehydrogenase (17ß-HSD) and cytochrome P450 aromatase (P450arom) in ovaries were detected by immunohistochemistry. The expression levels of 3ß-HSD, 17ß-HSD and P450arom were detected by RT-PCR and Western blot. The results showed that the serum levels of estrogen and testosterone of PCOS group were significantly higher than those of the NC group. There was no significant difference of serum progesterone level between the PCOS and NC groups. Compared with the NC group, the PCOS group showed increased mRNA and protein expressions of both 3ß-HSD and 17ß-HSD, as well as reduced P450arom mRNA and protein expressions. These results suggest that 3ß-HSD and 17ß-HSD, but not P450arom, may participate in the ovarian hormonal regulation in the present rat model of PCOS.

[Effects of Panax notoginseng saponins on pneumocyte apoptosis and c-Jun N-terminal kinase in lung ischemia/reperfusion injury].

The aim of the present study is to investigate the effects of Panax notoginseng saponins (PNS) on pneumocyte apoptosis and apoptosis-related protein, as well as c-Jun N-terminal kinase (JNK) in lung ischemia/reperfusion (I/R) injury. Thirty Wistar rats were randomly divided into control group, I/R group and PNS group. The unilateral lung I/R model was replicated by obstruction of left lung hilus for 30 min and reperfusion for 120 min in vivo. The rats in PNS group were given intraperitoneal injection of PNS at 60 min before ischemia and 10 min before reperfusion. Some lung tissues sampled at the end of the experiment were assayed for wet/dry weight ratio (W/T). The expressions of phosphorylated JNK (p-JNK) and JNK protein were detected by Western blot. The expressions of Bcl-2, Bax and Caspase-3 protein were detected by immunocytochemistry techniques. The pneumocyte apoptotic index (AI) was detected by terminal deoxynuleotidy1 transferase mediated dUTP nick end labeling (TUNEL). The morphological and ultrastructure changes were observed under light microscope and electron microscope, and the injured alveolus rate (IAR) was counted as well. The results showed that compared to control group, I/R group showed increased expressions of p-JNK, Bcl-2, Bax and Caspase-3 protein (all P < 0.01), decreased ratio of Bcl-2/Bax (P < 0.05), and increased values of AI, W/T and IAR (all P < 0.01). Moreover, light microscope and electron microscope showed serious morphological and ultrastructure injury in I/R group. Compared to I/R group, PNS group showed markedly decreased expressions of p-JNK, Bax and Caspase-3 protein (all P < 0.01), increased expression of Bcl-2 protein and ratio of Bcl-2/Bax (both P < 0.01), and lower values of AI, W/T and IAR (all P < 0.01). Meanwhile, light morphological and ultrastructure injury was found to be alleviated in PNS group. These results suggest that PNS can protect lung tissue from I/R injury, and the mechanism may correlate with suppressing JNK signal pathway, up-regulating the ratio of Bcl-2/Bax which results in inhibition of Caspase-3 dependent apoptosis.

[The protective function and mechanism of notoginsenoside Rb1 against hypoxia hypercapnia-induced pulmonary vasoconstriction].

OBJECTIVE: To explore the protective function and mechanism of notoginsenoside Rb1 against hypoxia hypercapnia-induced pulmonary vasoconstriction (HHPV). METHODS: The pulmonary artery smooth muscle cells of healthy male SD rats were primarily cultured and the second to the fifth subcultured cells were incubated with 8, 40, and 100 mg/L notoginsenoside Rb1 respectively under the hypoxia-hypercapnia condition (1% O2 and 6% CO2). The cells were harvested for 24 h. The phosphated extracellular signal-regulated kinase (p-ERK) protein expression of the cells was detected by Western blot. The mRNA expressions of ERK1 and ERK2 were detected using half quantitative reverse transcription polymerase chain reaction (RT-PCR). RESULTS: The expression of p-ERK protein, the mRNA expressions of ERK1 and ERK2 were weakly positive in the control group. Their expressions in the hypoxia-hypercapnia group were obviously enhanced (P < 0.01). After intervention of Rb1 at different concentrations, their expressions were obviously lowered (P < 0.05, P < 0.01) in a dose-dependent manner. The optimal effects were obtained at the dose of 100 mg/L. The expression of p-ERK protein was significantly positively correlated with mRNA expressions of ERK1 and ERK2 in notoginsenoside Rbl-treated groups (r = 0.500, P < 0.01; r = 0.977, P < 0.01). CONCLUSIONS: ERK1/2 pathway might play a role in the rat HHPV. Notoginsenoside Rb, could alleviate HHPV by inhibiting the ERK1/2 pathway.

Downregulation of tumor protein 53-inducible nuclear protein 1 expression in hepatocellular carcinoma correlates with poor prognosis.

The expression of tumor protein 53-inducible nuclear protein 1 (TP53INP1) is upregulated in certain cancers and downregulated in others. However, its expression in hepatocellular carcinoma (HCC) is not clear. The present study aimed to investigate the expression and prognostic value of TP53INP1 and its association with clinicopathological parameters in HCC. TP53INP1 expression in HCC tissue samples was examined via immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction. Expression was categorized as high or low. The correlations of TP53INP1 expression with clinical characteristics and patients' prognoses were determined. TP53INP1 was frequently decreased in HCC tissues compared with adjacent non-tumorous liver tissues. This decreased expression was significantly associated with American Joint Committee on Cancer stage (P=0.014) and vascular invasion (P=0.024). Kaplan-Meier analysis further revealed that recurrence-free survival (RFS) (P=0.001) and overall survival (OS) (P=0.002) were significantly worse among patients with low TP53INP1 expression than among those with high TP53INP1 expression. In addition, multivariate analyses revealed that TP53INP1 was an independent predictor of OS [hazard ratio (HR)=2.680, 95% confidence interval (CI)=1.087-6.608, P=0.032) and RFS (HR=2.284, 95% CI=1.157-4.511, P=0.017). In conclusion, the expression of TP53INP1 was decreased in HCC, and TP53INP1 downregulation was an independent predictor of poor prognosis in patients with HCC.

[Protective effect of tetramethylpyrazine and L-arginine on rats with acute myocardial infarction].

OBJECTIVE: To compare the protective effects of tetramethylpyrazine (TMP) alone and TMP and L-arginine (TMP-LA) combination on rats with acute myocardial infarction (AMI), and to explore its mechanism. METHODS: The rat model of AMI was established by via caudal vein injection of pituitrin. Experimental animal groups of normal, model, TMP treated and TMP-LA (via abdominal cavity and caudal vein respectively) treated groups were established. Expression of P- and E-selectin, serum creatine phosphokinase (CK) and troponin T (TnT), and marrow peroxidase (MPO) concentration in myocardial tissue were determined by immunohistochemical stain. RESULTS: As compared with the normal group, serum CK and TnT level, and MPO concentration in myocardial tissue were significantly higher in the model group (P < 0.01), with P- and E-selectin significantly up-regulated (P < 0.01). As compared with the model group, the above-mentioned parameters in the TMP or TMP-LA treated group was significantly lower (P < 0.05). CONCLUSION: Combined use of TMP and LA showed obvious synergism in treating AMI, by way of multi-link inhibition on expression of adhesive factors and decrease of leucocyte infiltration.

[Protective effects and mechanism of SP600125 on lung ischemia/reperfusion injury in rats].

OBJECTIVE: To investigate the protective effects and mechanism of SP600125-specificity inhibitor of c-Jun N-terminal kinase (JNK)on lung ischemia /reperfusion injury in rats. METHODS: The unilateral lung ischemia/reperfusion model was replicated in vivo. Rats were randomly divided into three groups (n = 10): control group, ischemia/reperfusion group ( I/R group) and ischemia/reperfusion + SP600125 group (SP600125 group). The lung tissues sampled at the end of each experiment were assayed for wet/dry weight ratio (W/D),the injured alveoli rate (IAR), the expression of phosphorylation JNK (p-JNK) and JNK protein were detected by Western blot, the expression of Bcl-2, Bax, Caspase3 protein were detected by immunocytochemistry techniques, the pneumocyte apoptosis index (AI) was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end abeling(TUNEL), the ultrastructure changes were observed under electron microscope. RESULTS: Compared to I/R group, the expression of p-JNK, Bcl-2, Bax and caspase-3 protein were markedly decreased (all P < 0.01), the expression of Bcl-2 protein and the ratio of Bcl-2/Bax were markedly increased in SP600125 group(all P < 0.01). The value of AI, W/D, IAR showed significantly lower than those in I/R group (all P <0.01). Meanwhile, light morphological and ultrastructure injury were found in SP600125 group. CONCLUSION: SP600125 can suppress JNK signal pathway, up-regulate the ratio of Bcl-2/Bax to inhibit Caspase-3 dependent apoptosis, so that it protects lung tissue from ischemia/reperfusion injury.

[Effect of ligustrazine and L-arginine on function of mitochondria in myocardium after ischemia/reperfusion injury of myocardium in rabbits].

AIM: To study the effect of ligustrazine (LGT) and L-arginine(L-Arg)on function of mitochondria in myocardium after myocardial ischemia/reperfusion injury (MI/RI). METHODS: 50 rabbits were randomly divided into five groups (n=10): Control group(A), MI/R group(B), MI/R + LGT group (C), MI/R+ L-Arg group (D), MI/R+ LGT + L-Arg group (E). The mitochondrial respiratory function, Ca2+ concentration ([Ca2+]m), malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were deter mined. Meanwhile, the contents of ATP and EC in the myocardial tissue were measured, respectively. RESULTS: It was found that mitochondrial respiratory control rate (RCR), state 3 (ST3), SOD in C, D, E group were higher than those of B group, state 4 (ST4), [Ca2+]m, MDA were lower than those of B group, ATP and EC levels of myocardial tissue were higher than those in B group; and there were not significant differences between E and A group of above. CONCLUSION: LGT and IL-Arg can improve function of mitochondria in myocardium after ischemia/reperfusion injury of myocardium in rabbits by decreasing oxygen free radical level and Ca" overload in the mitochondria.