Dataset Information

Amelioration of Benign Prostatic Hyperplasia by Costunolide and Dehydrocostus Lactone in Wistar Rats.

ABSTRACT:

Purpose

Sesquiterpene lactones, which are found in plants of the Asteraceae family, contain costunolide (CO) and dehydrocostus lactone (DCL) as indicator material. CO, in particular, has been reported to possess varied pharmacological activity, including anti-inflammatory, antibacterial, and antioxidant effects. This study was designed to characterize the effects of CO and DCL on benign prostate hyperplasia (BPH).

Materials and methods

Rats were injected subcutaneously daily for 8 weeks with 5 mg/kg testosterone to induce prostatic hyperplasia. Wistar rats were randomly divided into 5 groups of 10 animals each and received the following treatment: I. Normal control group; II. BPH-induced group; III. CO group (0.075 mg/kg); IV. DCL group (0.075 mg/kg); and V. Finasteride group (0.8 mg/kg). After treatment, changes in prostate weight and serum biochemical indices, serum dihydrotestosterone level, and mRNA levels of BCL2 were measured and histological examinations performed.

Results

Absolute and relative prostate weight in the indicator material treated groups, as well as prostate volume, decreased compared to those in the disease-induced group. Epithelial cell thickness increased significantly in the disease-induced group, with a significant decrease being observed in the CO group. The level of the anti-apoptotic protein BCL2 (B-cell lymphoma 2) tended to decrease to a greater extent in the DCL group than in the disease-induced group.

Conclusions

In this study, we confirmed that the indicator materials (CO and DCL) can help suppress the development of BPH.

SUBMITTER: Choi D

PROVIDER: S-EPMC7994664 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundMale lower urinary tract symptoms (LUTS) occur in more than half of men above 50 years of age. LUTS were traditionally attributed to benign prostatic hyperplasia (BPH) and therefore the clinical terminology often uses LUTS and BPH interchangeably. More recently, LUTS were also linked to fibrogenic and inflammatory processes. We tested whether osteopontin (OPN), a proinflammatory and profibrotic molecule, is increased in symptomatic BPH. We also tested whether prostate epithelial and stromal cells secrete OPN in response to proinflammatory stimuli and identified downstream targets of OPN in prostate stromal cells.MethodsImmunohistochemistry was performed on prostate sections obtained from the transition zone of patients who underwent surgery (Holmium laser enucleation of the prostate) to relieve LUTS (surgical BPH, S-BPH) or patients who underwent radical prostatectomy to remove low-grade prostate cancer (incidental BPH, I-BPH). Images of stained tissue sections were captured with a Nuance Multispectral Imaging System and histoscore, as a measure of OPN staining intensity, was determined with inForm software. OPN protein abundance was determined by Western blot analysis. The ability of prostate cells to secrete osteopontin in response to IL-1β and TGF-β1 was determined in stromal (BHPrS-1) and epithelial (NHPrE-1 and BHPrE-1) cells by enzyme-linked immunosorbent assay. Quantitative polymerase chain reaction was used to measure gene expression changes in these cells in response to OPN.ResultsOPN immunostaining and protein levels were more abundant in S-BPH than I-BPH. Staining was distributed across all cell types with the highest levels in epithelial cells. Multiple OPN protein variants were identified in immortalized prostate stromal and epithelial cells. TGF-β1 stimulated OPN secretion by NHPrE-1 cells and both IL-1β and TGF-β1 stimulated OPN secretion by BHPrS-1 cells. Interestingly, recombinant OPN increased the mRNA expression of CXCL1, CXCL2, CXCL8, PTGS2, and IL6 in BHPrS-1, but not in epithelial cell lines.ConclusionsOPN is more abundant in prostates of men with S-BPH compared to men with I-BPH. OPN secretion is stimulated by proinflammatory cytokines, and OPN acts directly on stromal cells to drive the synthesis of proinflammatory mRNAs. Pharmacological manipulation of prostatic OPN may have the potential to reduce LUTS by inhibiting both inflammatory and fibrotic pathways.