Preventive Effects of Monascus on Androgen-Related Diseases: Androgenetic Alopecia, Benign Prostatic Hyperplasia, and Prostate Cancer

Androgen-related diseases impair the well-being of many aging men. Unfortunately, the medications used to treat these diseases have many side effects. Therefore, there is a significant need for the development of novel drugs to treat androgen-related diseases. In this study, we investigated the effects of Monascus cursory extraction (M-CE) on androgen-related diseases, including androgenetic alopecia (AGA), benign prostatic hyperplasia (BPH) and prostate cancer. We found that M-CE suppressed baldness in male B6CBAF1/j mice. Furthermore, M-CE decreased PSA levels, indicating a protective effect of M-CE on testosterone-induced hyperplasia. M-CE also significantly decreased tumor volume and tumor incidence in an <i>N</i>-methyl-<i>N</i>-nitrosourea (MNU)/testosterone-induced rat prostate cancer model and markedly decreased dihydrotestosterone (DHT) but not testosterone. Additionally, PCNA expression was decreased in the prostate of rats treated with M-CE. These results suggest that M-CE could be a new potential therapeutic candidate for the treatment of androgen-related diseases

IR dose–response survival curves and cytotoxic effects resulting from MP and/or IR in PC-3 cells.

<p>(A) Chemical structure of MP. (B) Concentration-dependent effects of MP on the viability of PC-3 cells. Cells were treated with 5, 15, 25, 35 or 45 μM MP for 48 hrs. *, <i>p</i><0.05, MP versus control. (C) Cytotoxic effects in cells treated with IR (4 Gy) and/or MP (25 μM). #, <i>p</i><0.05, IR versus combined treatment. *, <i>p</i><0.05, MP versus combined treatment. (D) The radiation dose-response survival curves of PC-3 cells with or without MP. Data are presented as the mean ± standard deviation of three independent experiments.</p

Comet assay and ER stress induced by IR and/or MP in PC-3 cells. (A) EtBr staining of cells treated with IR (4

<p> <b>Gy) and MP (25 </b><b>μM).</b> The tails indicate DNA damage. (B) The effect of MP or IR alone or in combination for 48 hrs on average tail DNA. #, <i>p</i><0.05, IR versus combined treatment. *, <i>p</i><0.05, MP versus combined treatment.</p

Measurement of apoptosis and autophagy in PC-3 cells that received various treatments.

<p>(A) Early apoptosis, detected using an Annexin V apoptosis detection kit, was measured using flow cytometry. Cells were treated with IR (4 Gy) and MP (25 μM) for 48 hrs. (B) Development of AVOs in PC-3 cells. Detection of green and red fluorescence in AO-stained cells using flow cytometry. (C) Quantification of AVOs with AO-stained cells treated with IR (4 Gy) or MP (25 μM) alone or in combination using flow cytometry. #, <i>p</i><0.05, IR versus combined treatment. *, <i>p</i><0.05, MP versus combined treatment. Data are presented as the mean ± standard deviation of three independent experiments. (D) EM microphotographs of PC-3 cells treated with IR (4 Gy) and MP (25 μM) for 48 hrs. The <i>white arrows</i> point to autophagic vacuoles and autolysosomes. (E) Western blotting for LC3-I, LC3-II, p62/SQSTM1 and Atg5–12 in PC-3 cells. Cells were treated with IR (4 Gy) and MP (25 μM) for 48 hrs.</p

Tumor growth and body weight of tumor-bearing mice treated with IR (6

<p> <b>Gy) or MP (1 </b><b>mg/kg×6) alone or in combination.</b> (A) Body weight in nude mice, measured once per week. (B) Tumor volume in nude mice, measured every two days. Data are presented as the relative tumor volume (mean ± standard error) normalized to the initial tumor volume measured on day 0. (C) Direct observations of mice with tumors. Following experiments, the mice were sacrificed and the tumors were removed. (D) Measurement of tumor weight in the nude mice after sacrifice. (E) Immunohistochemical (IHC) and hematoxylin and eosin (H&E) staining of PC-3 mouse xenograft tissues. IHC was used to determine the expression levels of LC3 and p62/SQSTM1 (×100 objective magnification).</p

Comparison of tumor growth inhibition, tumor volume quadrupling time, and tumor growth delay time of PC-3 tumors in nude mice.

*<p> <b>Tumor growth inhibition rate was calculated based on the tumor volume on ay 10.</b></p><p> <b># </b><b><i>p</i></b><b> values for comparison of tumor growth delay time.</b></p

Six new metabolites produced by <i>Colletotrichum</i><i>aotearoa</i> 09F0161, an endophytic fungus isolated from <i>Bredia</i><i>oldhamii</i>

<div><p>Six new compounds, colletobredins A–D (<b>1</b>–<b>4</b>) and colletomelleins A and B (<b>5</b> and <b>6</b>), along with 12 previously identified compounds, were isolated from the culture broth of <i>Colletotrichum aotearoa</i> BCRC 09F0161, a fungal endophyte residing in the leaves of an endemic Formosan plant <i>Bredia oldhamii</i> Hook. f. (Melastomataceae). The structures of the new compounds were established by spectroscopic methods, including UV, IR, HR-ESIMS and extensive 1D and 2D NMR techniques. The effects of some isolates on the inhibition of nitric oxide (NO) production in lipopolysaccharide-activated murine macrophage RAW264.7 cells were evaluated. All these compounds inhibited NO production in activated macrophages without any cytotoxicity at a concentration of 100 μM. Of these isolates, <b>1</b> showed weak NO inhibitory activity with IC₅₀ value of 182.2 μM. To the best of our knowledge, this is the first report on isochroman glycoside metabolites (<b>1</b>–<b>4</b>) from the genus <i>Colletotrichum</i>.</p></div