Tadalafil Alleviates LPS-Induced Inflammation and Oxidative Stress of RWPE-1 Cell by Regulating the Akt/Nrf2 Signaling Pathway

Song, Xiu–Peng; Chen, Guodong; Li, Caixia; Yang, Chunyan; Deng, Yanfei

doi:10.1007/s10753-020-01384-w

Cited by 10 publications

(14 citation statements)

References 15 publications

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“…The simultaneous application of L-NAME reversed the effects of tadalafil, while there were no significant changes in the case of vardenafil. This supports the hypothesis regarding the contribution of the L-arginin/NO system on the effects of tadalafil and suggests that there may be another endothelial pathway for vardenafil-induced vascular effects [ 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 ]. It seems that tadalafil expresses its effects similarly to sildenafil, through the augmentation of NO synthase and cGMP levels, which points to the possibility that the cardiovascular dysfunctions that include decreased NOS activity may be alleviated by tadalafil treatment [ 30 , 31 ].…”

Section: Discussionsupporting

confidence: 86%

“…In one study, tadalafil decreased the levels of hydrogen peroxide, while in two others, sildenafil expressed the same effects on both the superoxide anion radical and hydrogen peroxide [ 21 , 22 , 23 ]. However, it should be taken into account that these studies were performed on men with erectile dysfunction and models with heart failure [ 24 , 25 , 26 , 27 ]. In both these cases, the basic antioxidant system was seriously damaged, which was not the case in our study.…”

Section: Discussionmentioning

confidence: 99%

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Changes in Left Ventricular Ejection Fraction and Oxidative Stress after Phosphodiesterase Type-5 Inhibitor Treatment in an Experimental Model of Retrograde Rat Perfusion

Krivokapic

Omarov²,

Živković

et al. 2023

Medicina

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Background and objectives: Taking into consideration the confirmed role of oxidative stress in ischemia/reperfusion injury and the insufficiency in knowledge regarding the phosphodiesterase 5 (PDE5)-mediated effects on the cardiovascular system, the aim of our study was to investigate the influence of two PDE5 inhibitors, tadalafil and vardenafil, with or without the addition of N(G)-nitro-L-arginine methyl ester (L-NAME), on oxidative stress markers, coronary flow and left ventricular function, both ex vivo and in vivo. Methods: This study included 74 male Wistar albino rats divided into two groups. In the first, 24 male Wistar rats were orally treated with tadalafil or vardenafil for four weeks in order to perform in vivo experiments. In the second, the hearts of 50 male Wistar albino were excised and perfused according to the Langendorff technique in order to perform ex vivo experiments. The hearts were perfused with tadalafil (10, 20, 50 and 200 nM), vardenafil (10, 20, 50 and 200 nM) and a combination of tadalafil/vardenafil and L-NAME (30 μM). The CF and oxidative stress markers, including nitrite bioaviability (NO2−), superoxide anion radical (O2−), and the index of lipid peroxidation, were measured in coronary effluent. Results: The L-arginin/NO system acts as the mediator in the tadalafil-induced effects on the cardiovascular system, while it seems that the vardenafil-induced increase in CF was not primarily induced by the NO system. Although tadalafil induced an increase in O2− in the two lowest doses, the general effects of both of the applied PDE5 inhibitors on oxidative stress were not significant. The ejection function was above 50% in both groups. Conclusions: Our results showed that both tadalafil and vardenafil improved the coronary perfusion of the myocardium and LV function by increasing the EF.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Changes in Left Ventricular Ejection Fraction and Oxidative Stress after Phosphodiesterase Type-5 Inhibitor Treatment in an Experimental Model of Retrograde Rat Perfusion

Krivokapic

Omarov²,

Živković

et al. 2023

Medicina

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“…In recent studies conducted on mice and human prostate cells, it was explained that LPS also caused oxidative stress besides inflammation. [ 52,53 ] MDA and PCO levels in pancreatic tissue were higher in the PDAC + LPS + CR group compared to the PDAC group. Similarly, GSH level and GST, GP‐X, and CAT activities were higher in the PDAC + LPS + CR group.…”

Section: Discussionmentioning

confidence: 83%

Influences of calorie restriction and lipopolysaccharide therapy on inflammation, cytokine response, and cell proliferation in pancreatic adenocarcinoma mouse model

Beydogan

Yazici

Bolkent

2022

J Biochem & Molecular Tox

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The study aimed to investigate the effects of lipopolysaccharide (LPS) alone and in combination with calorie restriction (CR) on the pancreatic tissues in C57BL/6 mice modeled with pancreatic ductal adenocarcinoma (PDAC). Forty male C57BL/6 mice (10‐13 weeks old) were divided into five groups; LPS, LPS + CR, PDAC, PDAC + LPS, and PDAC + LPS + CR. Nuclear factor kappa B (NF‐κβ), interleukin‐6 (IL‐6), and c‐Jun N‐terminal kinases (JNK) mRNA expression levels were measured in pancreatic tissues. NF‐κβ, IL‐6, JNK, and proliferating cell nuclear antigen (PCNA) peptide levels were determined by immunohistochemistry. Oxidative stress markers and antioxidant enzyme activities were determined spectrophotometrically. TH1/TH2 cytokine measurements were determined by a flow cytometer. It was detected that the number of PCNA immune + cells in the PDAC + LPS + CR group was significantly lower than in the PDAC and PDAC + LPS groups (p < 0.01, p < 0.05 respectively). PDAC + LPS + CR group's plasma interferon‐gamma (IFN‐γ), IL‐6, IL‐2, tumor necrosis factor‐alpha, IL‐3, and IL‐4 levels were found to be significantly lower than the PDAC group (p < 0.01, p < 0.001, p < 0.01, p < 0.05, p < 0.01, and p < 0.05 respectively). According to our findings, the combination of low‐dose LPS and 40% CR was found to be more effective in PDAC model mice.

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“…Pharmaceutical research in ED found that NFE2L2 was a promising target by regulating oxidative stress and inflammatory response in treating ED ( Draganski et al, 2018 ; Pierre et al, 2022 ). Similarly, in a model of chronic nonbacterial prostatitis, NFE2L2 was involved in the process that tadalafil alleviated inflammation and oxidative stress in RWPE-1 cells ( Song et al, 2021 ). These results propelled the interplay between ED and CP/CPPS.…”

Section: Discussionmentioning

confidence: 99%

Uncovering the genetic links of diabetic erectile dysfunction and chronic prostatitis/chronic pelvic pain syndrome

Yuan

Sun²,

Han³

et al. 2023

Front. Physiol.

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Background: Clinical associations between erectile dysfunction and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) have been noticed, but the common pathogenic mechanisms between them remain elusive. The aim of the study was to mine shared genetic alterations between ED and chronic prostatitis/chronic pelvic pain syndrome.Method: Transcriptome data of ED and chronic prostatitis/chronic pelvic pain syndrome-related genes (CPRGs) were retrieved from relevant databases and differentially expressed analysis was used to obtain significant CPRGs. Then function enrichment and interaction analyses were performed to show shared transcriptional signature, including gene ontology and pathway enrichment, the construction of protein-protein interaction (PPI) network, cluster analysis, and co-expression analysis. Hub CPRGs and key cross-link were selected by validating these genes in clinical samples, chronic prostatitis/chronic pelvic pain syndrome and ED-related datasets. Then the miRNA-OSRGs co-regulatory network was predicted and validated. Subpopulation distribution and disease association of hub CPRGs were further identified.Result: Differentially expressed analysis revealed 363 significant CPRGs between ED and chronic prostatitis/chronic pelvic pain syndrome, functioning in inflammatory reaction, oxidative stress, apoptosis, smooth muscle cell proliferation, and extracellular matrix organization. A PPI network containing 245 nodes and 504 interactions was constructed. Module analysis depicted that multicellular organismal process and immune metabolic process were enriched. 17 genes were screened in PPI via topological algorithms, and reactive oxygen species as well as interleukin-1 metabolism were regarded as the bridging interactive mechanism. After screening and validation, a hub-CPRG signature consisting of COL1A1, MAPK6, LPL, NFE2L2 and NQO1 were identified and associated miRNA were verified. These miRNAs played an important role in immune and inflammatory response likewise. Finally, NQO1 was identified as a key genetic link between ED and chronic prostatitis/chronic pelvic pain syndrome. It was predominately enriched in corpus cavernosum endothelial cell, and correlated with other male urogenital and immune system diseases tightly.Conclusion: We identified the genetic profiles as well as corresponding regulatory network underlying interaction between ED and chronic prostatitis/chronic pelvic pain syndrome via multi-omics analysis. These findings expanded a new understanding for the molecular mechanism of ED with chronic prostatitis/chronic pelvic pain syndrome.

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Tadalafil Alleviates LPS-Induced Inflammation and Oxidative Stress of RWPE-1 Cell by Regulating the Akt/Nrf2 Signaling Pathway

Cited by 10 publications

References 15 publications

Changes in Left Ventricular Ejection Fraction and Oxidative Stress after Phosphodiesterase Type-5 Inhibitor Treatment in an Experimental Model of Retrograde Rat Perfusion

Changes in Left Ventricular Ejection Fraction and Oxidative Stress after Phosphodiesterase Type-5 Inhibitor Treatment in an Experimental Model of Retrograde Rat Perfusion

Influences of calorie restriction and lipopolysaccharide therapy on inflammation, cytokine response, and cell proliferation in pancreatic adenocarcinoma mouse model

Uncovering the genetic links of diabetic erectile dysfunction and chronic prostatitis/chronic pelvic pain syndrome

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