Preventive Effect of Pentoxifylline on Acute Radiation Damage via Antioxidant and Anti-inflammatory Pathways

Hepgül, Gülçin; Tanrikulu, Sevda; Ünalp, Haluk Recai; Akgüner, Taner; Erbil, Yeşim; Olgaç, Vakur; Ademoğlu, Evin

doi:10.1007/s10620-009-0780-x

Cited by 36 publications

(25 citation statements)

References 32 publications

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“…Apoptotic bodies were clearly shown with 8 Gy irradiation levels. Similar findings were described by other authors (Driák et al, 2008;Hepgül et al, 2010;Wang et al, 2013) and the appearance of apoptotic bodies with high exposure levels was also previously reported (Deng et al, 2005;Akpolat et al, 2009;Wang et al, 2013).…”

Section: Discussionsupporting

confidence: 92%

“…Similar effects have been reported by other authors (Freeman and MacNaughton, 2000;Prasad et al, 2005;Zhou et al, 2006). Radiation-induced mucositis has also been associated with the release of inflammatory cytokines, such as TNF-␣ (Ong et al, 2010) and an increase in MPO activity (Hepgül et al, 2010) as well as a rise in serum DAO. The latter is highly located in small-intestinal mucosal cells and is released into the bloodstream when the intestinal mucosa is damaged (Zhou et al, 2011).…”

Section: Discussionsupporting

confidence: 82%

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A multi-component herbal preparation, STW 5, shows anti-apoptotic effects in radiation induced intestinal mucositis in rats

Khayyal

Abdel‐Naby

Abdel-Aziz³

et al. 2014

Phytomedicine

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 82%

A multi-component herbal preparation, STW 5, shows anti-apoptotic effects in radiation induced intestinal mucositis in rats

Khayyal

Abdel‐Naby

Abdel-Aziz³

et al. 2014

Phytomedicine

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“…These effects were decreased by noggin. Tumor necrosis factor is one of the most powerful inducers and promoters of inflammation [3], and NF- κ B both is activated by cytokines and induces the expression of inflammatory cytokines. This gives rise to the potential for NF- κ B activation to spread from cell to cell within a tissue and beyond [18].…”

Section: Resultsmentioning

confidence: 99%

“…Acute intestinal ischemia is a life-threatening vascular emergency; however, the improvement in recent years has been minimal, and its in-hospital mortality rate remains high at approximately 60%–80% [3, 4]. Although many studies have focused on I/R, the mechanisms have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Intestinal Mucosal Barrier Is Injured by BMP2/4 via Activation of NF-κB Signals after Ischemic Reperfusion

Chen

Xie

Luo

et al. 2014

Mediators of Inflammation

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Intestinal ischemic reperfusion (I/R) can cause dysfunction of the intestinal mucosal barrier; however, the mechanism of the intestinal mucosal barrier dysfunction caused by I/R remains unclear. In this study, using intestinal epithelial cells under anaerobic cultivation and an in vivo rat intestinal I/R model, we found that hypoxia and I/R increased the expression of BMP2/4 and upregulated BMP type Ia receptor and BMP type II receptor expression. We also found that exogenous BMP2/4 can activate the ERK and AKT signaling pathways in rat small intestine (IEC-6) cells, thereby activating NF-κB signaling, which leads to increased levels of inflammatory factors, such as TNF-α and IL-6. Furthermore, recombinant BMP2/4 decreased the expression of the tight junction protein occludin via the activation of the NF-κB pathway; these effects were abolished by treatment with the BMP-specific antagonist noggin or the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC). All these factors can destroy the intestinal mucosal barrier, thereby leading to weaker barrier function. On the basis of these data, we conclude that BMP2/4 may act as the pathogenic basis for intestinal mucosal barrier dysfunction when the intestines suffer an I/R injury. Our results provide background for the development pharmacologic interventions in the management of I/R injury.

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“…The mechanism underlying the antioxidant actions of pentoxifylline in NM-induced lung toxicity are unknown. Pentoxifylline has been reported to inhibit lipid oxidation and to interfere with oxygen radical mediated activation of the pro-inflammatory transcription factor, NFκB; it also prevents glutathione depletion and up-regulates glutathione peroxidase (Hepgul et al, 2010). It remains to be determined if these actions contribute in the protective activity of pentoxifylline against NM-induced oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Sunil

Vayas

Cervelli

et al. 2014

Experimental and Molecular Pathology

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Nitrogen mustard (NM) is a toxic alkylating agent that causes damage to the respiratory tract. Evidence suggests that macrophages and inflammatory mediators including tumor necrosis factor (TNF)α contribute to pulmonary injury. Pentoxifylline is a TNFα inhibitor known to suppress inflammation. In these studies, we analyzed the ability of pentoxifylline to mitigate NM-induced lung injury and inflammation. Exposure of male Wistar rats (250 g; 8–10 weeks) to NM (0.125 mg/kg, i.t.) resulted in severe histolopathological changes in the lung within 3 d of exposure, along with increases in bronchoalveolar lavage (BAL) cell number and protein, indicating inflammation and alveolar-epithelial barrier dysfunction. This was associated with increases in oxidative stress proteins including lipocalin (Lcn)2 and heme oxygenase (HO)-1 in the lung, along with pro-inflammatory/cytotoxic (COX-2+ and MMP-9+), and anti-inflammatory/wound repair (CD163+ and Gal-3+) macrophages. Treatment of rats with pentoxifylline (46.7 mg/kg, i.p.) daily for 3 d beginning 15 min after NM significantly reduced NM-induced lung injury, inflammation, and oxidative stress, as measured histologically and by decreases in BAL cell and protein content, and levels of HO-1 and Lcn2. Macrophages expressing COX-2 and MMP-9 also decreased after pentoxifylline, while CD163+ and Gal-3+ macrophages increased. This was correlated with persistent upregulation of markers of wound repair including pro-surfactant protein-C and proliferating nuclear cell antigen by Type II cells. NM-induced lung injury and inflammation were associated with alterations in the elastic properties of the lung, however these were largely unaltered by pentoxifylline. These data suggest that pentoxifylline may be useful in treating acute lung injury, inflammation and oxidative stress induced by vesicants.

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Preventive Effect of Pentoxifylline on Acute Radiation Damage via Antioxidant and Anti-inflammatory Pathways

Abstract: PTX appears to have a protective effect against radiation damage. This protective effect is mediated in part by decreasing both inflammatory reactions and oxidative stress.

Cited by 36 publications

References 32 publications

A multi-component herbal preparation, STW 5, shows anti-apoptotic effects in radiation induced intestinal mucositis in rats

A multi-component herbal preparation, STW 5, shows anti-apoptotic effects in radiation induced intestinal mucositis in rats

Intestinal Mucosal Barrier Is Injured by BMP2/4 via Activation of NF-κB Signals after Ischemic Reperfusion

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

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