[Efficacy of Kangshuailing Gao on benign prostatic hyperplasia in rats].

OBJECTIVE: To investigate the effect of Kangshuailing Gao (KG) on benign prostatic hyperplasia (BPH) in rats and its action mechanisms. METHODS: Fifty BPH model rats were randomized into five groups of equal number, BPH model control, finasteride control, and high-, medium- and low-dose KG, to be treated intragastrically with distilled water, finasteride solution at 0.52 mg/kg, and KG solution at 4.16, 2.08 and 1.04 g/kg respectively once a day for 30 days consecutively. Another 10 normal healthy rats were taken as blank controls. The rats were weighed once a week during the treatment. The wet weight and index of the prostate were obtained after treatment, followed by measurement of the contents of serum estradiol (E2) and dihydrotestosterone (DHT), testosterone (T) and hypoxia-inducible factor-1α (HIF-1α) in the prostatic tissue, and observation of histomorphological changes in the prostate under the light microscope. RESULTS: Compared with the BPH model control group, high- and medium-dose KG significantly reduced the prostate wet weight (ï¼»0.84 ± 0.08ï¼½ vs ï¼»0.69 ± 0.04ï¼½ and ï¼»0.71 ± 0.07ï¼½ g, P < 0.01), the prostatic index (ï¼»0.28 ± 0.03ï¼½% vs ï¼»0.20 ± 0.02ï¼½% and ï¼»0.22 ± 0.03ï¼½%, P < 0.01), and the levels of T (ï¼»4.63 ± 1.25ï¼½ vs ï¼»2.44 ± 0.47ï¼½ and ï¼»2.91 ± 0.69ï¼½ ng/L, P < 0.01) and DHT (ï¼»154.44 ± 20.25ï¼½ vs ï¼»88.23 ± 13.63ï¼½ and ï¼»90.52 ± 16.44ï¼½ nmol/L, P < 0.01), but increased the level of E2 (ï¼»0.95 ± 0.24ï¼½ vs ï¼»1.19 ± 0.14ï¼½ and ï¼»1.20 ± 0.22ï¼½ nmol/L, P < 0.01) in the serum. High-dose KG remarkably reduced the overexpression of HIF-1α in the prostate tissue of the BPH model rats (P < 0.01) and alleviated such BPH-related symptoms as epithelium thinning, intraglandular secretion reduction, and interstitial substance decrease. CONCLUSIONS: Kangshuailing Gao acted effectively on BPH in the model rats by reducing the androgen level, balancing the estrogen/androgen ratio, and downregulating the expression of HIF-1α in the prostate tissue.

The Protective Effect of Total Flavones from Rhododendron simsii Planch. on Myocardial Ischemia/Reperfusion Injury and Its Underlying Mechanism.

OBJECTIVES: Total flavones from Rhododendron simsii Planch. (TFR) are the effective part extracted from the flowers of Rhododendron simsii Planch. and have obvious protective effects against cerebral ischemic or myocardial injuries in rabbits and rats. However, their mechanism of cardioprotection is still unrevealed. Therefore, the present study was designed to investigate the effect of TFR on myocardial I/R injury and the underlying mechanism. METHODS: TFR groups were treated by gavage once a day for 3 days at a dose of 20, 40, and 80 mg/kg, respectively, and then the model of myocardial I/R injury was established. Myocardial infarction, ST-segment elevation, and the expression of UTR, ROCK1, ROCK2, and p-MLC protein in rat myocardium were determined at 90 min after reperfusion. UTR siRNA in vivo transfection and competition binding assay method were used to study the relationship between the protective effect of TFR and UTR. RESULTS: The expression of UTR protein markedly decreased in myocardium of UTR siRNA transfection group rats. TFR could significantly reduce the infarct size and inhibit the increase of RhoA activity and ROCK1, ROCK2, and p-MLC protein expressions both in WT and UTR knockdown rats. The reducing rate of TFR in myocardial infarction area, RhoA activity, and ROCK1, ROCK2, and p-MLC protein expressions in UTR knockdown rats decreased markedly compared with that in WT rats. In addition, TFR had no obvious effect on the increase of ΣST in UTR knockdown rats in comparison with that in model group. In particular, TFR could significantly inhibit the combination of [125I]-hu-II and UTR, and IC50 was 0.854 mg/l. CONCLUSIONS: The results indicate that the protective effect of TFR on I/R injury may be correlated with its blocking UTR and the subsequent inhibition of RhoA/ROCK signaling pathway.

The effect of ethyl acetate extract from persimmon leaves on Alzheimer's disease and its underlying mechanism.

BACKGROUND: Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorders characterized by neuronal loss in the brain and cognitive impairment. AD is now considered to be the third major cause of death in developed countries, after cardiovascular disease and cancer. Persimmon leaves are used as a popular folk medicine to treat hypertension, angina and internal haemorrhage in Cyangbhina, and it has been reported that ethyl acetate extract of persimmon leaves (EAPL) displays a potential therapeutic effect on neurodegenerative diseases. HYPOTHESIS/PURPOSE: This study was designed to investigate the effects of EAPL on AD, to clarify the possible mechanism by which EAPL exerts its beneficial effects and prevents AD, and to determine the major constituents involved. STUDY DESIGN: AD model was established by bilateral injection of Aß1-42 into the hippocampus of rats. The cognitive performance was determined by the Morris water maze and step-down tests. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), apoptosis, total and phosphorylated c-Jun NH2-terminal kinase (JNK/p-JNK), caspase-3, Bax and Bcl-2 were determined. In addition, a sensitive and reliable LC-QTOF-MS method was applied to identify the major compounds present in EAPL. RESULTS: EAPL at doses of 200mg/kg, 400mg/kg could markedly reduce the latency, significantly increase the time in the first quadrant and number of the target crossing times in Morris water maze test, markedly increase the latency and reduce the number of errors in the step-down test, significantly inhibit the reductions in SOD and GSH-Px activities, and increase the level of MDA. In addition, EAPL treatment attenuated neuronal apoptosis in the hippocampus, reduced the expression of p-JNK, caspase-3, and the relative ratio of Bax/Bcl-2. Meanwhile, 32 constituents were identified by LC-QTOF-MS/MS assays. CONCLUSION: The results indicate that EAPL has a potent protective effect on cognitive deficits induced by Aß in rats and this effect appears to be associated with the regulation of the antioxidative defense system and the mechanism of mitochondrial-mediated apoptosis. Furthermore, analysis of the LC-MS data suggests that flavonoids and triterpenoids may be responsible for the potential biological effects of EAPL.