Curcumin attenuates prostatic hyperplasia caused by inflammation
            <i>via</i>
            up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor

Liu, Yuhang; Wang, Zhaohui; Gan, Yu; Chen, Xiang; Zhang, Bo; Chen, Zhi; Liu, Peihuan; Li, Bingsheng; Feng, Ru; He, Yao

doi:10.1080/13880209.2021.1953539

Cited by 9 publications

(10 citation statements)

References 41 publications

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“…Previous research has demonstrated that these growth factors are associated with angiogenic growth [ 20 ], stromal extracellular matrix accumulation [ 21 ] and prostatic enlargement [ 22 ] in animal BPH models. Another animal study by Liu et al found that treatment with Curcumin reduced PV by reduction of the epithelial–mesenchymal transition on histology [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…Regardless of the causes of prostatic inflammation, the latter is characterized by a large infiltration of T-cells and the expression of a variety of pro-inflammatory cytokines [ 24 , 25 ]. Liu et al demonstrated that administration of Curcumin in mice caused a lower expression of pro-inflammatory cytokines such as IL-6 and TNF-a as compared to the control group, indicating that Curcumin alleviates inflammation in an induced BPH mouse model [ 15 ]. The role of inflammation in BPH was also confirmed in three randomized clinical trials where non-steroidal anti-inflammatory drugs were administered in patients with LUTS/BPH in comparison with placebo for 4–24 weeks [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…In a rat study, the Curcumin group demonstrated a decreased expression of growth factors (VEGF, TGF-ß1, and IGF1) in the prostatic tissue and a significantly lower prostate weight and volume compared to the testosterone-induced BPH group [ 14 ]. In another animal study, the effect of Curcumin was confirmed in vivo on reducing prostate size and the levels of proinflammatory cytokines (IL-6 and TNF-a) and exhibited in vitro attenuated prostatic cell proliferation [ 15 ]. Therefore, Curcumin may inhibit the effects of androgens and inflammation of the prostate.…”

Section: Introductionmentioning

confidence: 99%

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Efficacy of 1-Year Cavacurmin® Therapy in Reducing Prostate Growth in Men Suffering from Lower Urinary Tract Symptoms

Milanese

Agostini

Angelis

et al. 2023

JCM

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We aim to assess the effect of Cavacurmin® on prostate volume (PV), lower urinary tract symptoms (LUTS) and micturition parameters in men after 1 year of therapy. From September 2020 to October 2021, data from 20 men with LUTS/benign prostatic hyperplasia and PV ≥40 mL who were on therapy with α1-adrenoceptor antagonists plus Cavacurmin® were retrospectively compared with 20 men on only α1-adrenoceptor antagonists. Patients were evaluated at baseline and after 1 year using the International Prostate Symptom Score (IPSS), prostate-specific antigen (PSA), maximum urinary flow (Qmax) and PV. A Mann–Whitney U-test and Chi-square were used to assess the difference between the two groups. A comparison of paired data was performed with the Wilcoxon signed-rank test. Statistical significance was set at p-value < 0.05. There was no statistically significant difference in baseline characteristics between the two groups. At the 1-year follow-up, PV [55.0 (15.0) vs. 62.5 (18.0) mL, p = 0.04)], PSA [2.5 (1.5) ng/mL vs. 3.05 (2.7) vs. p = 0.009] and IPSS [13.5 (3.75) vs. 18 (9.25) p = 0.009] were significantly lower in the Cavacurmin® group. Qmax was significantly higher in the Cavacurmin® group [15.85 (2.9) vs. 14.5 (4.2), p = 0.022]. PV was reduced to 2 (5.75) mL in the Cavacurmin® group from baseline, while it increased to 12 (6.75) mL in the α1-adrenoceptor antagonists group (p < 0.001). PSA decreased in the Cavacurmin® group [−0.45 (0.55) ng/mL], whereas it increased in the α1-adrenoceptor antagonists group [0.5 (0.30) ng/mL, p < 0.001]. In conclusion, one-year Cavacurmin® therapy was able to block prostate growth with a concomitant decrease in PSA value from baseline. The association of Cavacurmin® with α1-adrenoceptor antagonists had a more beneficial effect compared to patients on α1-adrenoceptor antagonists alone but this needs further larger studies to be confirmed, particularly in the long-term.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Efficacy of 1-Year Cavacurmin® Therapy in Reducing Prostate Growth in Men Suffering from Lower Urinary Tract Symptoms

Milanese

Agostini

Angelis

et al. 2023

JCM

View full text Add to dashboard Cite

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“…Aberrant proliferation of stromal and epithelial cells causes glandular hypertrophy and bladder outlet obstruction [ 33 ]. Considering that EMT and the balance between epithelial proliferation and apoptosis are central events during BPH [ 34 , 35 ], m 6 A modification might act on BPH etiology and pathology by affecting these molecular and cellular events.…”

Section: Discussionmentioning

confidence: 99%

METTL3 promotes prostatic hyperplasia by regulating PTEN expression in an m6A-YTHDF2-dependent manner

Yao

Huang

et al. 2022

Cell Death Dis

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Uncontrolled epithelial cell proliferation in the prostate transition zone and the hyper-accumulation of mesenchymal-like cells derived from the epithelial-mesenchymal transition (EMT) of prostatic epithelium are two key processes in benign prostatic hyperplasia (BPH). m6A RNA modification affects multiple cellular processes, including cell proliferation, apoptosis, and differentiation. In this study, the aberrant up-regulation of methylase METTL3 in BPH samples suggests its potential role in BPH development. Elevated m6A modification in the prostate of the BPH rat was partially reduced by METTL3 knockdown. METTL3 knockdown also partially reduced the prostatic epithelial thickness and prostate weight, significantly improved the histological features of the prostate, inhibited epithelial proliferation and EMT, and promoted apoptosis. In vitro, METTL3 knockdown decreased TGF-β-stimulated BPH-1 cell proliferation, m6A modification, and EMT, whereas promoted cell apoptosis. METTL3 increased the m6A modification of PTEN and inhibited its expression through the reading protein YTHDF2. PTEN knockdown aggravated the molecular, cellular, and pathological alterations in the prostate of BPH rats and amplified TGF-β-induced changes in BPH-1 cells. More importantly, PTEN knockdown partially abolished the improving effects of METTL3 knockdown both in vivo and in vitro. In conclusion, the level of m6A modification is elevated in BPH; the METTL3/YTHDF2/PTEN axis disturbs the balance between epithelial proliferation and apoptosis, promotes EMT, and accelerates BPH development in an m6A modification-related manner.

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“…This conclusion has been verified in many experiments. Taking CUR as an example, CUR alleviates inflammatory diseases by reducing major markers of inflammation, such as IL-6 and TNF-α, malondialdehyde, sensitive C-reactive protein, MCP-1 ( 114 – 116 ). The anti-inflammatory effect of dietary polyphenols is the basis of their biological activity.…”

Section: Discussionmentioning

confidence: 99%

Regulation of dietary polyphenols on cancer cell pyroptosis and the tumor immune microenvironment

et al. 2022

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Cancer is a major public health problem that threatens human life worldwide. In recent years, immunotherapy has made great progress in both clinical and laboratory research. But the high heterogeneity and dynamics of tumors makes immunotherapy not suitable for all cancers. Dietary polyphenols have attracted researchers' attention due to their ability to induce cancer cell pyroptosis and to regulate the tumor immune microenvironment (TIME). This review expounds the regulation of dietary polyphenols and their new forms on cancer cell pyroptosis and the TIME. These dietary polyphenols include curcumin (CUR), resveratrol (RES), epigallocatechin gallate (EGCG), apigenin, triptolide (TPL), kaempferol, genistein and moscatilin. New forms of dietary polyphenols refer to their synthetic analogs and nano-delivery, liposomes. Studies in the past decade are included. The result shows that dietary polyphenols induce pyroptosis in breast cancer cells, liver cancer cells, oral squamous cells, carcinoma cells, and other cancer cells through different pathways. Moreover, dietary polyphenols exhibit great potential in the TIME regulation by modulating the programmed cell death protein 1(PD-1)/programmed death-ligand 1 (PD-L1) axis, enhancing antitumor immune cells, weakening the function and activity of immunosuppressive cells, and targeting tumor-associated macrophages (TAMs) to reduce their tumor infiltration and promote their polarization toward the M1 type. Dietary polyphenols are also used with radiotherapy and chemotherapy to improve antitumor immunity and shape a beneficial TIME. In conclusion, dietary polyphenols induce cancer cell pyroptosis and regulate the TIME, providing new ideas for safer cancer cures.

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Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor

Abstract: He (2021) Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membranebound inhibitor,

Cited by 9 publications

References 41 publications

Efficacy of 1-Year Cavacurmin® Therapy in Reducing Prostate Growth in Men Suffering from Lower Urinary Tract Symptoms

Efficacy of 1-Year Cavacurmin® Therapy in Reducing Prostate Growth in Men Suffering from Lower Urinary Tract Symptoms

METTL3 promotes prostatic hyperplasia by regulating PTEN expression in an m6A-YTHDF2-dependent manner

Regulation of dietary polyphenols on cancer cell pyroptosis and the tumor immune microenvironment

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