Luteolin Treatment Protects against Renal Ischemia-Reperfusion Injury in Rats

Hong, Xin; Zhao, Xiaojing; Wang, Gang; Zhang, Zhengliang; Pei, Honghong; Liu, Zhong

doi:10.1155/2017/9783893

Cited by 50 publications

(46 citation statements)

References 38 publications

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“…Recently, it was demonstrated that luteolin effectively suppresses IL-1β, TNF-α, IL-6 and IL-8 secretion from PBMC from healthy donors incubated with LPS [203], confirming reports showing that luteolin reduces IL-6 and TNF-α secretion in LPS-stimulated RAW 264.7 macrophages [190]. Hong et al evaluated the anti-inflammatory effects of luteolin in renal I/R injury in Sprague-Dawley rats and demonstrated that this natural compound attenuated serum and renal TNF-α, IL-1β and IL-6, and the renal HMGB1 and NF-κB expression levels in I/R rats [204]. In addition, luteolin significantly reduced the endoplasmic reticulum stress and renal cell apoptosis caused by renal I/R injury [204].…”

Section: Flavanonessupporting

confidence: 53%

“…Hong et al evaluated the anti-inflammatory effects of luteolin in renal I/R injury in Sprague-Dawley rats and demonstrated that this natural compound attenuated serum and renal TNF-α, IL-1β and IL-6, and the renal HMGB1 and NF-κB expression levels in I/R rats [204]. In addition, luteolin significantly reduced the endoplasmic reticulum stress and renal cell apoptosis caused by renal I/R injury [204]. Recently, Ding et al demonstrated that luteolin attenuates atherosclerosis in high-fat fed apoE-/-mice by alleviating inflammation through inhibition of signal transducer and STAT3 [205].…”

Section: Flavanonesmentioning

confidence: 99%

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Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

et al. 2020

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Atherosclerosis is the main process behind cardiovascular diseases (CVD), maladies which continue to be responsible for up to 70% of death worldwide. Despite the ongoing development of new and potent drugs, their incomplete efficacy, partial intolerance and numerous side effects make the search for new alternatives worthwhile. The focus of the scientific world turned to the potential of natural active compounds to prevent and treat CVD. Essential for effective prevention or treatment based on phytochemicals is to know their mechanisms of action according to their bioavailability and dosage. The present review is focused on the latest data about phenolic compounds and aims to collect and correlate the reliable existing knowledge concerning their molecular mechanisms of action to counteract important risk factors that contribute to the initiation and development of atherosclerosis: dyslipidemia, and oxidative and inflammatory-stress. The selection of phenolic compounds was made to prove their multiple benefic effects and endorse them as CVD remedies, complementary to allopathic drugs. The review also highlights some aspects that still need clear scientific explanations and draws up some new molecular approaches to validate phenolic compounds for CVD complementary therapy in the near future.In the last decade the scientific researchers turned their attention to phytochemicals, as effective, safe and low-cost natural bioactive compounds for CVD treatment.Dyslipidemia consists of increased blood concentrations of total cholesterol (TC), low density lipoproteins-cholesterol (LDL-C) and/or triglycerides (TG), and decreased high density lipoproteins-cholesterol (HDL-C) [6]. The lipid metabolism is complex and the candidate mechanisms that could generate dyslipidemia include: (i) excessive dietary lipid absorption in the small intestine; (ii) packing of exogenous lipids with cholesterol and fatty acids produced de novo in the liver and their secretion as very low density lipoproteins (VLDL); (iii) hydrolysis of TG from VLDL by lipases and their conversion into LDL, which are taken up by the peripheral tissues through LDL receptor (LDL-R) and scavenger receptors; (iv) diminished production of HDL by the liver and small intestine, thereby decreasing reverse cholesterol transport (RCT) from the peripheral tissues to the liver; (v) lowered excess cholesterol excretion from the liver into gallbladder or to the intestinal lumen through the ATP-binding cassette G5 and G8 transporters (ABCG5/G8) that facilitate trans-intestinal cholesterol efflux (TICE). Dyslipidemia is associated with the accumulation of LDL in the sub-endothelium of the artery wall. At this site, LDL undergoes oxidative modifications (oxLDL) that trigger inflammatory responses, and is taken up by the monocyte-derived macrophages infiltrated in the sub-endothelium which thus become lipid-loaded foam cells, the hallmark of atheroma development [7]. Until now, the most effective lipid-lowering treatment for hyperlipidemic patients was the statin therapy. But recen...

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Section: Flavanonessupporting

confidence: 53%

Section: Flavanonesmentioning

confidence: 99%

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

et al. 2020

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“…Reperfüzyon sonucunda dokuda oluşan SOR'lar lipid peroksidasyonuna ve hücre hasarına yol açmaktadır (7). Bu nedenle İ/R hasarının şiddetini azaltmaya yönelik olarak yapılan deneysel çalışmalarda çok sayıda antioksidan ve antiinflammatuar maddenin etkisi araştırılmaktadır (18)(19)(20) (10). Bir başka çalışmada ise nizatidinin MPO-H2O2-Cl-sisteminde üretilen güçlü bir klorlayıcı oksidan olan hipokloröz asiti (HOCl) büyük ölçüde temizlediği ifade edilmektedir (25).…”

Section: Discussionunclassified

Effect of Nizatidine on Renal Ischemia-Reperfusion Damage

Mammadov¹,

Bilgin²

2019

Van Med J

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Sistemik hipotansiyon, hipovolemik şok, kardiyak arest, aortun klempajı ve renovasküler cerrahi gibi çeşitli nedenlerle böbreklerin kan akımının kesilmesi veya azalması sonucunda böbrek dokusunda iskemi gelişmektedir (1, 2). Dokuların iskemiye uzun süre maruz kalması ciddi organ fonksiyon bozukluklarına ve hatta hücre ölümüne neden olmaktadır (3). İskemiye bağlı hasarın, dokuda enerji depolarının boşalması ve toksik maddelerin birikiminden kaynaklandığı öne sürülmektedir (4). Bu nedenle, iskemik hasarın rejenere edilmesi için dokunun yeniden kanlanmasının sağlanması oldukça önem arz etmektedir. Ancak reperfüzyon sonucu iskemili dokuya, arteryel kan ile aşırı miktarda sunulan moleküler oksijen (O2), aşırı serbest oksijen radikallerinin oluşmasına ve ÖZET Amaç: İskemili dokuya yapılacak olan ilk müdahale dokunun yeniden kanlanmasını sağlamaktır. Ancak, reperfüzyonda iskemili dokuya, arteryel kanla bol miktarda oksijen sunulmaktadır. Dokuda artan moleküler oksijen aşırı serbest oksijen radikalinin oluşmasına ve oksidatif strese yol açmaktadır. Bu da iskemi/reperfüzyon (I/R) hasarının azaltılmasında antioksidan tedavinin yararlı olabileceğini göstermektedir. Çalışmamızda, böbrek I/R hasarına etkisini araştıracağımız niazatidin, peptik ülser tedavisinde kullanılan H2 reseptör antagonisti antiülser bir ilaçtır. Nizatidinin sitoprotektif etkisinin antioksidan özelliğinden kaynaklandığı bilinmektedir. Literatürlerde, nizatidinin böbrek I/R hasarı üzerindeki koruyucu etkisine dair bir çalışmaya rastlanmadı. Çalışmamızın amacı, nizatidinin sıçanlarda I/R ile oluşturulan oksidatif böbrek hasarına etkisini araştırmaktır. Gereç ve Yöntem: Bu çalışmada albino Wistar türü 18 adet erkek sıçan renal iskemi-reperfüzyon (RİR), 50 mg/kg nizatidin + renal iskemi-reperfüzyon (NIR-50) ve şam operasyonu uygulanacak (SG) gruplara ayrıldı. Bulgular: Biyokimyasal deney sonuçlarımız İ/R işlemi gerçekleştirilen RİR grubunun böbrek dokusunda malondialdehit (MDA) ve myeloperoksidaz (MPO) gibi oksidatif stres belirteçlerinin SG grubuna göre anlamlı (p<0.0001) yükseldiğini, süperoksit dismutaz (SOD) ve glutatyon peroksidaz (GPO) gibi endojen antioksidanların ise anlamlı (p<0.0001) düştüğünü göstermiştir. Nizatidin böbrek dokusunda MDA ve MPO'nun artmasını, SOD ve GPO'nun ise azalmasını anlamlı olarak (p<0.0001) önlemiştir. Sonuç: Deney sonuçlarımız, nizatidinin böbrek dokusunu İ/R hasarına karşı koruduğunu ortaya koymaktadır.

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“…The grading system was shown as the following scoring: 0 (normal kidney); 1 (0-5% injury, minimal damage); 2 (5-25% injury, mild damage); 3 (25-75% injury, moderate damage); and 4 (75-100% injury, severe damage). 16,17 Immunohistochemistry Immunohistochemical analysis was performed using the Histone Simple Stain Kit (Nichirei, Tokyo, Japan), according to the manufacturer's instructions. Paraffin-embedded sections were deparaffinised with xylene and then rehydrated in a descending series of ethanol washes.…”

Section: Morphologic Analysismentioning

confidence: 99%