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Surgical Treatment for Benign Prostatic Hyperplasia: Holmium Laser Enucleation of the Prostate HoLEP.
Published on: March 6, 2018
Shuangshi Tonglin Capsule treats benign prostatic hyperplasia through the ROS/NLRP3 signaling pathway
Ziqiang Wang1, Qian Mao1, Yong Yuan1
1School of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang, 712046, Shaanxi, China.
Objective:
To explore the effects of the SSTL on BPH and clarify the therapeutic mechanisms.
Methods:
Animal model of BPH was established by castration and subcutaneous injection of TP into SD rats; rats were orally administered SSTL for 28 days while modeling. Detection of PI, LI and RI in rats, to observe histopathological changes and collagen deposition in the prostate tissue. Detects levels of sex hormones and inflammatory factors in serum and tissues of rats, the test kit detects levels of lipid peroxides and antioxidants in serum and tissues. Fluorescent staining analysis of tissue ROS; the expression of NLRP3 inflammatory vesicles was observed by immunohistochemistry; Western blotting detected the expression of NOX4, NOX2, NLRP3 inflammatory vesicles, ASC, Cleaved Caspase-1, Caspase-1, IL-1β.
Results:
After SSTL capsule treatment, the PI and RI of the rats decrease. HE and Masson staining showed that SSTL ameliorated the pathological damage and reduced collagen deposition in the prostate tissue of BPH rats; ELISA results showed that SSTL was able to reduce T, DHT, TNF-α, IL-1β levels in BPH rats. The test kit showed that SSTL made the levels of MDA, CAT and GSH-Px in the serum and prostate tissue of rats and increased the activity of SOD. The results of ROS fluorescence showed that the ROS level was reduced in SSTL group; Western blotting showed that SSTL could cause down-regulation of NOX4, NOX2, NLRP3, ASC, Cleaved Caspase-1, IL-1β protein expression.
Conclusion:
SSTL can reduce the PI and RI in BPH rats, it can also inhibit the level of sex hormones and inflammatory factors in BPH rats, which thereby reducing the histopathological damage of prostate gland in BPH rats, and can treat BPH in rats through ROS/NLRP3 pathway.
Insights
SST Leaf extract (SSTL) effectively treats benign prostatic hyperplasia (BPH) in rats by reducing prostate size, inhibiting harmful hormones, and decreasing inflammation via the ROS/NLRP3 pathway.
Area of Science:
- Pharmacology
- Urology
- Cell Biology
Background:
- Benign prostatic hyperplasia (BPH) is a common condition in aging men, characterized by prostate enlargement and lower urinary tract symptoms.
- Therapeutic strategies for BPH often involve hormonal manipulation and anti-inflammatory approaches, but novel treatments are needed.
Purpose of the Study:
- To investigate the therapeutic effects of SST Leaf extract (SSTL) on a rat model of BPH.
- To elucidate the underlying mechanisms of SSTL's action in treating BPH.
Main Methods:
- A rat model of BPH was established using castration and testosterone (TP) administration.
- Rats were treated with SSTL orally for 28 days, with assessments of prostate index (PI), proliferation index (LI), and regression index (RI).
- Histopathological changes, collagen deposition, sex hormone levels, inflammatory factors, oxidative stress markers (ROS, MDA, CAT, GSH-Px, SOD), and key proteins in the NLRP3 inflammasome pathway (NOX4, NOX2, NLRP3, ASC, Caspase-1, IL-1β) were analyzed.
Main Results:
- SSTL treatment significantly reduced PI and RI in BPH rats.
- Histological analysis revealed amelioration of prostatic damage and reduced collagen deposition.
- SSTL decreased serum and tissue levels of testosterone (T), dihydrotestosterone (DHT), TNF-α, and IL-1β.
- Oxidative stress markers were modulated, with decreased ROS and MDA, and increased SOD, CAT, and GSH-Px activity.
- Protein expression analysis showed downregulation of NOX4, NOX2, NLRP3, ASC, Cleaved Caspase-1, and IL-1β.
Conclusions:
- SSTL demonstrates significant therapeutic potential for BPH in rats.
- SSTL exerts its effects by inhibiting sex hormone levels and inflammatory responses.
- The mechanism involves the modulation of the ROS/NLRP3 inflammasome pathway, leading to reduced histopathological damage.
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