Infiltration of inflammatory factors induced penile damage in chronic prostatitis

Wang, K; Mao, Weipu; Ni, Jinliang; Xie, Jinbo; Yin, Lei; Zhang, Houliang; Zhang, Tao; Xu, Tianmin; Peng, Bo

doi:10.1111/and.14113

Cited by 4 publications

(1 citation statement)

References 18 publications

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“…Subsequently, 4 µm sections were sliced from the embedded tissues and subjected to IHC staining, following a previously reported protocol. [ 23 ] The sections were incubated with anti‐MLC1 and anti‐KI67 antibodies. Finally, images were captured using a microscope (Leica Microsystems, Mannheim, Germany).…”

Section: Methodsmentioning

confidence: 99%

MLC1 Overexpression Inhibits Tumor Progression through PI3K/AKT Signal Pathway in Prostate Cancer

Wu,

Ni,

Zhang

et al. 2023

Advanced Biology

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Prostate cancer (PC) is a prevalent malignancy in males, characterized by high morbidity and mortality. Despite MLC1 being established as a key mediator in tumor progression, its role in PC remains unexplored. This study aims to validate MLC1's anti‐tumor effects and uncover potential mechanisms. MLC1's clinical significance is assessed using data from The Cancer Genome Atlas and the Genotype‐Tissue Expression databases. MLC1 expression is significantly reduced in PC samples compared with the adjacent normal tissues. MLC1 expression correlates negatively with tumor metastasis and positively with the survival of patients with PC. In vitro, up‐regulating MLC1 effectively inhibits tumor progression by curtailing proliferation, infestation, and migration through the deactivation of the PI3K/AKT signaling pathway. Conversely, down‐regulating MLC1 promotes PC progression, a phenomenon alleviated by the PI3K/AKT inhibitor, Gefitinib. Furthermore, the anti‐tumor function of MLC1 is corroborated by a reduction in tumor volume compared with the negative control in vivo. This study confirms the anti‐tumor effects of MLC1 via in vitro and in vivo experiments, demonstrating its potential mechanism of inhibiting the PI3K/AKT signaling pathway.

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Section: Methodsmentioning

confidence: 99%

MLC1 Overexpression Inhibits Tumor Progression through PI3K/AKT Signal Pathway in Prostate Cancer

Wu,

Ni,

Zhang

et al. 2023

Advanced Biology

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Composition‐Reinforced Polydopamine Nanoenzyme for Improved Impairment of Prostatitis‐Damaged Sexual Behavior and Enhanced Anti‐Prostate Cancer

Wang,

Mao,

Song

et al. 2024

Adv Funct Materials

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Inflammation is pivotal in the pathogenesis and progression of the most challenging diseases and even cancer. Nanomedicine‐based strategy can be referred as a distinct solution to this complicated clinical obstacle by proposing an elaborated combination of effective therapeutic performances on inflammation and cancer. Herein, 2,2,6,6‐tetramethylpiperidine‐1‐oxyl doped polydopamine nanoparticles, termed as TPDA NPs, with the significantly improved reactive oxygen/nitrogen species (RO/NSs) scavenging performance and enhanced photothermal efficiency are designed and synthesized by constructing donor‐acceptor pairs, for prostate diseases treatment including anti‐inflammation and anti‐tumor. Benefiting from mimicking multi‐natural enzymes, including superoxide dismutase, catalase, peroxidase, and glutathione peroxidase, TPDA NPs can inhibit the NF‐κB signaling pathways by downregulating the CD36 expression for the treatment of oxidative stress‐induced prostatitis. Especially, TPDA NPs can improve the prostatitis‐associated impairment of sexual behavior. By virtue of the enhanced photothermal‐conversion efficiency, TPDA NPs ablate prostate cancer and simultaneously decrease inflammatory reaction. Therefore, this work provides a “three birds with one shot” paradigm to utilize rationally designed TPDA NPs for efficient management of prostate diseases.

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Calycosin protects against chronic prostatitis in rats via inhibition of the p38MAPK/NF-κB pathway

Wang,

He,

Liu

et al. 2023

Open Medicine

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Currently, the effect and molecular mechanism of calycosin, the main active ingredient of Qinshi Simiao San, which can alleviate chronic prostatitis (CP), on CP remain unclear. This study aimed to elucidate the potential mechanism of action of calycosin in CP in a rat CP model. The prostate tissue morphology was evaluated based on hematoxylin–eosin staining. Enzyme-linked immunosorbent assay was conducted to evaluate inflammatory cytokine and immune factor levels (secretory immunoglobulin A [SIgA]; immunoglobulin G [IgG]) in prostate tissues and serum. Additionally, representative biomarkers of oxidative stress, including malondialdehyde, superoxide dismutase, and catalase were detected using detection kits, and reactive oxygen species release was evaluated using immunofluorescence staining. Furthermore, the p38 mitogen-activated protein kinase (p38MAPK)/NF-kappaB (NF-κB) signaling pathway was analyzed by western blotting. The results showed that calycosin substantially ameliorated the pathological damage to prostate tissues of the CP rats. Moreover, calycosin significantly downregulated interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha, IgG, and SIgA levels. Furthermore, we found that calycosin considerably suppressed oxidative stress and inhibited the activation of the p38MAPK/NF-κB signaling pathway in rats with CP. In summary, our findings revealed that calycosin protects against CP in rats by inhibiting the p38MAPK/NF-κB pathway.

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Infiltration of inflammatory factors induced penile damage in chronic prostatitis

Cited by 4 publications

References 18 publications

MLC1 Overexpression Inhibits Tumor Progression through PI3K/AKT Signal Pathway in Prostate Cancer

MLC1 Overexpression Inhibits Tumor Progression through PI3K/AKT Signal Pathway in Prostate Cancer

Composition‐Reinforced Polydopamine Nanoenzyme for Improved Impairment of Prostatitis‐Damaged Sexual Behavior and Enhanced Anti‐Prostate Cancer

Calycosin protects against chronic prostatitis in rats via inhibition of the p38MAPK/NF-κB pathway

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