Sod mimetics are coming of age

Salvemini, Daniela; Riley, Dennis P.; Cuzzocrea, Salvatore

doi:10.1038/nrd796

Cited by 250 publications

(191 citation statements)

References 99 publications

Supporting

Mentioning

185

Contrasting

Order By: Relevance

“…High levels of oxidants enhance TGF-β production (26), activate protease and promote the fibrotic response. Certain antioxidants, including SOD, have been observed to inhibit collagen deposition and protect the lungs in a range of animal models (27). As shown in Fig.…”

Section: A B a B Cmentioning

confidence: 94%

Apigenin protects against bleomycin-induced lung fibrosis in rats

Chen

Zhao

2015

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Apigenin is a non-toxic and non-mutagenic flavone that exists abundantly in numerous herbs and vegetables. Apigenin exerts anti-proliferative and anti-inflammatory properties. The aim of the present study was to investigate the effects of apigenin on bleomycin-induced lung fibrosis in rats. A single intratracheal instillation of bleomycin (5 mg/kg) was administered and rats were sacrificed on 7 and 28 days post bleomycin instillation. The instillation of bleomycin resulted in decreased body weight and an increase in the lung index. In addition, bleomycin administration increased the hydroxyproline content, myeloperoxidase (MPO) activity, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β levels and decreased the superoxide dismutase (SOD) activity in the rat lung tissues. Excessive collagen deposits were detected in the lung tissues in bleomycin-treated rats compared with normal control rats. Notably, the oral administration of apigenin (10, 15 and 20 mg/kg/day) appeared to prevent the fibrotic process. The treatment suppressed the increases in hydroxyproline content, MPO activity, TNF-α and TGF-β levels and attenuated the reduction of SOD activity that were induced by bleomycin. Furthermore, excessive collagen deposition was inhibited by the apigenin treatment. Collectively, these results suggest that apigenin may function as a potent anti-inflammatory and anti-fibrotic agent against bleomycin-induced lung fibrosis.

show abstract

Section: A B a B Cmentioning

confidence: 94%

Apigenin protects against bleomycin-induced lung fibrosis in rats

Chen

Zhao

2015

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

“…In a therapeutic approach, administration of endogenous SOD would only offer antioxidant activity in the extracellular space and not within the cell itself. As a result, several smaller molecular mass SOD mimetics that imitate the endogenous SOD functions have been developed [111]. Since radiation creates ROS directly within the cell due to the ionization of water molecules and mitochondria within the cell produce ROS, and inflammation creates ROS outside the cell, it is important that protective agents be effective in both locations (Figure 1-7).…”

Section: Protection Against Oxidative Damage -Sod and Sod Mimeticsmentioning

confidence: 99%

“…Many studies have also focused on protecting against oxidative damage and reducing ROS levels using agents similar to SOD. SODs are metalloproteins that can dismutate superoxide anions to less reactive hydrogen peroxide and oxygen without extra input of cellular energy [111].…”

Section: Protection Against Oxidative Damage -Sod and Sod Mimeticsmentioning

confidence: 99%

Effects of genistein following fractionated lung irradiation in mice

Para¹,

Bezjak²,

Yeung³

et al. 2009

Radiotherapy and Oncology

View full text Add to dashboard Cite

Radiation therapy for lung cancer and cancers of the upper thorax is limited by side effects to normal tissue of the lung. An understanding of mechanisms leading to radiation induced lung damage is essential to developing protective agents. In this thesis an anti-oxidant and anti-inflammatory agent Genistein was investigated for its potential to affect DNA damage, tissue inflammation, functional deficits and survival. We hypothesized that chronic oxidative stress and the subsequent inflammatory response play a key role in the development of major lung complications, radiation pneumonitis and fibrosis. If side effects of radiation could be reduced, then larger doses could be delivered to the tumor with a better chance of eradicating the disease.ii Acknowledgements

show abstract

“…For example, amifostine is a potent scavenger of free radicals 71 . Superoxide dismutase (SOD) and various SOD mimetics are also being pursued as potential radioprotective strategies 72 . The vitamin E analog, gamma-tocotrienol is the most potent non-toxic natural radioprotective compound discovered to date 73 .…”

Section: Preclinical Research To Prevent Radiation Enteropathymentioning

confidence: 99%

Correction: Radiation enteropathy—pathogenesis, treatment and prevention

Hauer‐Jensen¹,

Denham²,

Andreyev³

2014

Nat Rev Gastroenterol Hepatol

View full text Add to dashboard Cite

There has been only modest change in cancer incidence and mortality during the past several decades, but the number of cancer survivors has almost tripled during the same period. With an increasing cohort of cancer survivors, efforts to prevent, diagnose, and manage side effects of cancer therapy in general and, specifically those of radiation therapy have intensified. Many cancer survivors have undergone radiation therapy of tumors in the pelvis or abdomen, thus rendering the bowel at risk for injury. In fact, the current prevalence of patients with long term radiation-induced intestinal side effects exceeds that of ulcerative colitis and Crohn's disease combined. Significant progress toward reducing toxicity of radiation therapy has been made by the introduction of so-called dose-sculpting treatment techniques, which allow more precise delivery of the radiation beam. Moreover, new insight into the underlying pathophysiology have resulted in an improved understanding of mechanisms of radiation-induced bowel toxicity and in development of new diagnostic strategies and management opportunities. This article discusses the pathogenesis of early and delayed radiation-induced bowel toxicity, reviews current management options, and outlines priorities for future research. The gastroenterologist by adding insight into molecular and cellular mechanisms of related bowel disorders can substantially strengthen these efforts.

show abstract

Sod mimetics are coming of age

Cited by 250 publications

References 99 publications

Apigenin protects against bleomycin-induced lung fibrosis in rats

Apigenin protects against bleomycin-induced lung fibrosis in rats

Effects of genistein following fractionated lung irradiation in mice

Correction: Radiation enteropathy—pathogenesis, treatment and prevention

Contact Info

Product

Resources

About