The angiotensin converting enzyme inhibitor captopril attenuates testosterone-induced benign prostatic hyperplasia in rats; a mechanistic approach

Mostafa, Fatma; Mantawy, Eman M.; Azab, Samar S.; El‐Demerdash, Ebtehal

doi:10.1016/j.ejphar.2019.172729

Cited by 16 publications

(9 citation statements)

References 61 publications

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“…Consistently, the ELISA results indicated the rise in the TNF‐α, iNOS, and IL‐1β levels in the serum of rats after BPH modeling, which was curbed by SIRT3 overexpression. In addition, Mostafa et al 20 revealed that TP significantly increased prostate weight, PCNA activity, and reduced Bax/Bcl‐2 ratio, p53, and caspase‐3 activity. Likewise, restoration of SIRT3 reduced the ratio of prostate to body weight, PCNA‐positive cells as well as potentiated apoptosis in prostate tissues of BPH rats.…”

Section: Discussionmentioning

confidence: 98%

SIRT3 affects mitochondrial metabolic reprogramming via the AMPK–PGC‐1α axis in the development of benign prostatic hyperplasia

Wang

Li³

et al. 2021

The Prostate

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BackgroundSirtuin 3 (SIRT3) has been reported to share an association with mitochondrial metabolic reprogramming. However, the molecular mechanism underlying is not well understood, especially in benign prostatic hyperplasia (BPH). Therefore, the purpose of this study was to research whether SIRT3 can affect the progression of BPH via the regulation of mitochondrial metabolic reprogramming.MethodsFollowing the development of a rat model of BPH using testosterone propionate (TP), we extracted prostate tissues from sham‐operated and BPH rats. Subsequently, bioinformatics prediction was used to screen the genes differentially expressed in BPH. To verify the role played by SIRT3 in BPH, we injected AAV9‐SIRT3 into rats, followed by TP treatment. Prostate epithelial cells (PEC) were treated with TP to assess the mitochondrial morphology, mitochondrial membrane potential, and expression of enzymes related to the oxidative phosphorylation pathway after SIRT3 expression alteration. Finally, we examined the expression of AMPK–PGC‐1α pathway in tissues and cells.ResultsSIRT3 was reduced in the prostate tissues of BPH rats. After overexpression of SIRT3, mitochondrial morphology was more stable in prostate tissues of BPH rats and in TP‐treated PEC, with significant increases in mitochondrial membrane potential and in the expression of oxidative phosphorylation‐related enzymes in the cytoplasm. Moreover, SIRT3 significantly activated the AMPK–PGC‐1α signaling pathway, which maintained the stability of mitochondrial membrane potential as well as mitochondrial structure, thus alleviating the symptoms of BPH.ConclusionSIRT3 maintained the stability of mitochondrial membrane potential as well as mitochondrial structure by activating the AMPK–PGC‐1α pathway, thereby alleviating the symptoms of BPH.

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Section: Discussionmentioning

confidence: 98%

SIRT3 affects mitochondrial metabolic reprogramming via the AMPK–PGC‐1α axis in the development of benign prostatic hyperplasia

Wang

Li³

et al. 2021

The Prostate

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“…Some researchers administered ACEI (captopril) to mice with testosterone-induced BPH, and ACEI was able to significantly inhibit prostate cell remodeling. Also, the expression of inflammatory cytokines like IL-8 and TNF-α in the ACEI group was significantly lower than in the BPH group [17]. It is reasonable to speculate that the expression of AngII could be upregulated after androgen supplementation activates the RAS system in the prostate, which in turn activates the NF-κB inflammatory pathway and causes increased secretion of inflammatory cytokines.…”

Section: The Combined Effect Of Androgens and Inflammationmentioning

confidence: 95%

“…After injecting testosterone subcutaneously into mice and constructing a BPH mouse model, it was observed that the prostates of mice were enlarged significantly, the morphological structure of prostate cells changed, and the stromal cells and epithelial cells became hypertrophic. The expression of antiapoptotic gene Bcl-2 in the prostates of mice in the BPH group was significantly upregulated, while the expression of apoptosis-related genes, such as Bax, p53, and caspase-3, were downregulated, resulting in cellular proliferation and BPH occurrence [16,17]. Leimgruber et al [18] proved in vitro that the proliferation capacity of rat prostate smooth muscle cells (pSMCs) was significantly enhanced, and the expression of proliferationrelated protein p-ERK1/2 increased after testosterone treatment.…”

Section: The Role Of Androgens In Bphmentioning

confidence: 99%

“…DHT can upregulate the expression of inflammatory factor TNF-α by stimulating AR on activated macrophages. When constructing a BPH mouse model using exogenous androgens, it was found that the classic inflammation pathway NF-κB was activated in the prostate tissue of mice injected with testosterone subcutaneously, and the expressions of IL-8, TNF-α, and COX-2 were significantly upregulated [16,17]. The microenvironment in the 4…”

Section: The Combined Effect Of Androgens and Inflammationmentioning

confidence: 99%

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Review of the Roles and Interaction of Androgen and Inflammation in Benign Prostatic Hyperplasia

Tong

Zhou

2020

Mediators of Inflammation

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The lower urinary tract symptoms (LUTSs) and acute urinary retention (AUR) caused by benign prostatic hyperplasia (BPH) can seriously affect the quality of life of elderly men. Studies suggest that both androgens and inflammation greatly influence the occurrence and development of BPH in most patients. These two factors combined can also affect each other, leading to pathological changes in the stromal and epithelial tissue of the prostate transition zone in BPH patients. DHT in the prostate tissue of BPH patients may activate a chronic inflammatory response in the prostate, amplifying the expression of inflammatory factors and upregulating the proliferation ability of prostate tissue.

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“…It's well-documented that NO is important for the correlation between inflammation and BPH [ 6 , 66 ]. Prostatic inflammatory mediators like TNF-α, IL-1β, IL-2, -4,-6, 8, TGF-β, COX-2, and IFN- ϒ are of crucial importance for BPH [ 12 , 13 , 66 , 70 , 71 ]. Experimentally, several studies have investigated the elements that prevent the secretion of inflammatory cytokines [ 66 , 72 ].…”

Section: Discussionmentioning

confidence: 99%

Berberine ameliorates testosterone-induced benign prostate hyperplasia in rats

Shabani

Kalantari‬

Kalantar

et al. 2021

BMC Complement Med Ther

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Introduction Benign prostatic hyperplasia (BPH) is a major urologic problem that mostly develops in older males. Oxidative stress and inflammation influence the occurrence of BPH. Berberine (BBR) is a natural ingredient that has antioxidant and anti-inflammatory properties. The current research aims at examining the effects of BBR on testosterone-stimulated BPH in rats. Methods Animals were randomly categorized to six groups. In the control group, normal saline and olive oil were injected as the vehicle. BPH group: received testosterone (3 mg/kg, subcutaneous, 28 days), BPH + BBR groups; received BBR (25 and 50 mg/kg, p.o, 28 days), BPH + finasteride groups: received finasteride (1 mg/kg, p.o, 28 days), BBR (50 mg/kg, p.o, alone) was administered for subjects in the BBR group. On the 29th day, after anesthesia, cervical dislocation was used to kill the subjects. Serum concentration of testosterone and dihydrotestosterone was measured and prostate tissues were excised and used for biochemical, inflammation, and histological analysis. Results BBR prevented increased serum concentrations of testosterone and dihydrotestosterone. BBR considerably reduced BPH-stimulated oxidative stress and inflammation through preventing the rise in lipid peroxidation and nitrite concentration and declined the accumulations of pro-inflammatory cytokines (e.g. interleukin 1β and tumor necrosis factor α) and declining the depletion rate of GSH and the function of catalase and superoxide dismutase. Histopathological investigations reported that administration of BBR could suppress testosterone-stimulated BPH. Conclusion This study demonstrated that BBR could significantly prevent the development of BPH in rats.

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The angiotensin converting enzyme inhibitor captopril attenuates testosterone-induced benign prostatic hyperplasia in rats; a mechanistic approach

Cited by 16 publications

References 61 publications

SIRT3 affects mitochondrial metabolic reprogramming via the AMPK–PGC‐1α axis in the development of benign prostatic hyperplasia

SIRT3 affects mitochondrial metabolic reprogramming via the AMPK–PGC‐1α axis in the development of benign prostatic hyperplasia

Review of the Roles and Interaction of Androgen and Inflammation in Benign Prostatic Hyperplasia

Berberine ameliorates testosterone-induced benign prostate hyperplasia in rats

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