ABSTRACT
OBJECTIVE: To investigate the effect of Kangquan Recipe (, KQR) on bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI) expression and its mechanism in rats with benign prostatic hyperplasia (BPH). METHODS: Forty-eight male Sprague-Dawley rats were divided into 6 groups using a random number table, with 8 in each group: the normal group (normal saline 10 mL/kg), the model group (normal saline 10 mL/kg), the finasteride group (0.5 mg/kg), the low-dose KQR group (3.5 g/kg), the middle-dose KQR group (7 g/kg), and the high-dose KQR group (14 g/kg). The 40 rats were subcutaneously injected with testosterone propionate after castration for 30 days to establish the BPH rat model except for those in the normal group. At the same time, the corresponding drugs were administered by gavage for 30 consecutive days. The effects of different doses of KQR on the protate wet weight, prostate volume and prostate index (PI) were observed. The changes in histopathology were monitored with hematoxylin-eosin staining. BAMBI protein and mRNA expression contents were determined by Western blot and quantitative real-time polymerase chain reaction, respectively. RESULTS: All doses of KQR could decrease prostatic epithelial tissue proliferation. Compared to the model group, the high and middle-dose KQR significantly reduced prostate wet weight, prostate volume and PI; increased BAMBI protein expression in the hypothalamus, pituitary and prostate tissue; all doses of KQR up-regulated BAMBI mRNA expression in serum, prostatic fluid and prostate tissue (P<0.05 or P<0.01). CONCLUSIONS: KQR could inhibit the proliferation of rat prostatic tissue, promote BAMBI protein expression in the hypothalamic-pituitary-prostate of rats with BPH; and increase BAMBI mRNA expression in the blood, prostatic fluid and prostate tissue of rats with BPH, showing a dose-effect relationship. KQR can be used as a potential drug for the treatment of BPH.
Subject(s)
Prostatic Hyperplasia , Animals , Drugs, Chinese Herbal , Hypothalamus , Male , Membrane Proteins , Prostatic Hyperplasia/drug therapy , Rats , Rats, Sprague-Dawley , TestosteroneABSTRACT
Alzheimer's disease (AD) is the most common neurodegenerative disorder associated with aging. There are currently no effective treatments for AD. Bazhu decoction (BZD), a traditional Chinese medicine (TCM) formula, has been employed clinically to alleviate AD. However, the underlying molecular mechanisms are still unclear. Here we found that middle- and high-doses of BZD ameliorated the behavioral aspects of 5xFAD transgenic mice in elevated plus maze, Y maze and Morris water maze tests. Moreover, BZD reduced the protein levels of BACE1 and PS1, resulting in a reduction of Aß plaques. We also identified a beneficial effect of BZD on oxidative stress by attenuating MDA levels and SOD activity in the brains of 5xFAD mice. Together, these results indicate that BZD produces a dose-dependent positive effect on 5xFAD transgenic mouse model by decreasing APP processing and Aß plaques, and by ameliorating oxidative damage. BZD may play a protective role in the cognitive and anxiety impairments and may be a complementary therapeutic option for AD.
ABSTRACT
Gypenosides (GP) are a type of traditional Chinese medicine (TCM) extracted from plants and commonly applied for treatment of metabolic diseases. This study aims to explore the effects of GP extracts on alleviating non-alcoholic fatty liver disease (NAFLD). In this experiment, C57BL/6â¯J mice were randomly assigned into normal diet control (ND), HFHC (high-fat and high-cholesterol) and HFHCâ¯+â¯GP (GP) groups. Mice in HFHC group were fed HFHC diet combined with fructose drinking water for 12 weeks to induce the animal model of NAFLD, followed by ordinary drinking water until the end of the experiment. In the HFHCâ¯+â¯GP group, mice were fed HFHC diet combined with fructose drinking water for 12 weeks, followed by GP-containing drinking water till the end. Mouse body weight was measured weekly. After animal procedures, mouse liver and serum samples were collected. It is shown that GP administration reduced body weight, enhanced the sensitivity to insulin resistance (IR) and decreased serum levels of ALT, AST and TG in NAFLD mice. In addition, GP treatment alleviated steatohepatitis, and downregulated ACC1, PPARγ, CD36, APOC3 and MTTP levels in mice fed with HFHC diet. Furthermore, GP treatment markedly improved intestinal microbiota, and reduced relative abundance ratio of Firmicutes / Bacteroidetes in the feces of NAFLD mice. Our results suggested that GP alleviated NAFLD in mice through improving intestinal microbiota.
Subject(s)
Disease Progression , Gastrointestinal Microbiome/drug effects , Non-alcoholic Fatty Liver Disease/drug therapy , Non-alcoholic Fatty Liver Disease/microbiology , Animals , Biodiversity , Body Weight/drug effects , Diet, High-Fat , Down-Regulation/drug effects , Gynostemma/chemistry , Hyperlipidemias/complications , Hyperlipidemias/drug therapy , Insulin Resistance , Intestines/drug effects , Intestines/pathology , Lipid Metabolism/drug effects , Liver/drug effects , Liver/pathology , Mice, Inbred C57BL , Non-alcoholic Fatty Liver Disease/blood , Non-alcoholic Fatty Liver Disease/complications , Organ Size/drug effects , Plant Extracts/chemistry , Plant Extracts/pharmacology , Plant Extracts/therapeutic useABSTRACT
BACKGROUND: Kangquan Recipe (KQR) is a traditional Chinese medicine compound made by our research group for the treatment of benign prostatic hyperplasia (BPH). Whether KQR can treat BPH as a single drug or play a role in the treatment of BPH in combination therapy needs further study. AIM OF THE STUDY: To investigate the effect of KQR on the expression of TGF-ß/Smad signaling pathway-related factors in rats with BPH. In-depth analysis revealed the relevant signal transduction mechanism by which KQR acts to treat BPH. MATERIALS AND METHODS: Forty-eight male Sprague-Dawley rats were randomly divided into six groups of 8 rats each. In addition to the control group, 40 rats were castrated and then injected with testosterone propionate to form a prostatic hyperplasia model. After 30 days, three groups received different concentrations of KQR (14 g/kg, 7 g/kg, and 3.5 g/kg), and the finasteride group received 0.5 mg/kg finasteride. The BPH group and the control group received the same volume of saline. All groups were treated for a total of 30 days. Rat body weight, prostate volume, wet weight, index, histology, and the mRNA and protein levels of TGF-ß, TGF-ßR1, TGF-ßR2, p-Smad2, p-Smad3, BAMBI, E-cadherin, and N-cadherin in the prostate tissue were measured after the end of treatment. RESULTS: Compared with the control group, the BPH group had increased prostate wet weight, volume, and index, and the histology showed significant BPH. Compared with the BPH group, the three KQR groups and the finasteride group all had varying levels of reduction in the prostate wet weight, volume, and index of the prostate and varying degrees of improvement in the histological manifestations of BPH. KQR downregulates the mRNA and/or protein expression of TGF-ß, TGF-ßR1, TGF-ßR2, p-Smad2, p-Smad3, and N-cadherin protein in prostate tissue and increases the mRNA and protein expression of BAMBI and E-cadherin protein. CONCLUSIONS: In the model of BPH induced by testosterone propionate after castration, KQR can inhibit the conduction of the TGF-ß/Smad signaling pathway by upregulating the expression of BAMBI protein and reversing EMT in rat prostate tissue.