Effects of melatonin on streptozotocin-induced diabetic liver injury in rats

Güven, Aysel; Yavuz, Özlem; Cam, Meryem; Ercan, Feríha; Bukan, Neslihan; Comunoglu, Cem; Gökçe, Fatih

doi:10.1016/j.acthis.2006.03.005

Cited by 89 publications

(69 citation statements)

References 33 publications

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“…Besides, it has been reported that diabetes increased oxidative stress in many organs, especially in the liver (29). Subsequently increased MDA levels were in concordance with the results of the previous studies on liver (43,44). CAPE is a potent antioxidant, which has been reported to prevent oxidative injury secondary to peroxidation (45).…”

Section: Discussionsupporting

confidence: 81%

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

Taşlıdere¹,

Gül²,

Elbe³

et al. 2016

BLL

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The aim of the present study was to clarify the role of oxidative stress in streptozotocin induced liver injury and the possible protective effect of caffeic acid phenethyl ester (CAPE) using histological and biochemical parameters. 32 male Wistar rats were divided into 4 groups as follows: Group 1: Control animals, Group 2: Control animals given CAPE Group 3: STZ-induced diabetic animals (DM group), Group 4: STZ-induced diabetic rats given CAPE (DM+CAPE group). All the injections started on the same day of single-dose STZ injection and continued for 20 days. At the end of this period, livers were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were signifi cantly increased compared with the control group. Signifi cant increases in tissue malondialdehyde (MDA) level and decreases in superoxide dismutase (SOD) and total glutathione (GSH) activities were detected in DM group. Administration of CAPE signifi cantly reduced these values. STZ-induced histopathological alterations including infl ammatory cell infi ltration around portal triad, congestion, loss of glycogen in the hepatocytes. Additionally, degenerative cellular alterations, such as numerous vacuolizations including myelinic fi gure formation, pyknotic nuclei with peripheral localization of heterochromatin condensation and mitochondrial elongation were observed in cytoplasm of hepatocytes. CAPE signifi cantly reduced these histopathological changes. Our results indicate that CAPE should be considered in the prevention of oxidative stress in diabetic liver (Tab. 3, Fig. 4, Ref. 47). Text in PDF www.elis.sk. KEY WORDS: caffeic acid phenethyl ester, streptozotocin, liver.

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Section: Discussionsupporting

confidence: 81%

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

Taşlıdere¹,

Gül²,

Elbe³

et al. 2016

BLL

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“…The hepatocytes' nuclei were generally enlarged and sometimes showed irregular contours and intranuclear inclusions. 20,21,25 In this study, we observed similar morphological changes in STZ-NA treated diabetic rat liver. In untreated diabetic rats and L-NNA treated diabetic rats, the nuclei of hepatocytes were enlarged.…”

Section: Histopatologysupporting

confidence: 70%

Antioxidant and Free Radical-Scavenging Properties of Stevia rebaudiana (Bertoni) Extracts and L-NNA in Streptozotocine-Nicotinamide Induced Diabetic Rat Liver

Özbayer¹,

Değirmenci²,

Kurt³

et al. 2011

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : Fre e ra di cal pro duc ti on is imp li ca ted in the pat ho ge ne sis of di a be tes mel li tus, in which seve ral path ways and dif fe rent mec ha nisms are shown to in vol ve in the pat hoph ysi o logy of the comp li ca ti ons. Thro ugh the ad mi nis tra ti on of ni co ti na mi de(NA) and strep to zo to cin(STZ), a mo del of hu man type II di a be tes can be in du ced in rats. The aim of this study was to de ter mi ne the ef fects of Ste vi a re ba u di a na (SrB) and L-NNA (N-nit ro-L-ar gi ni ne) in the for ma ti on of fre e ra di cals in STZ-NA in du ced type II di a be tic rats. M Ma a t te e r ri i a al l a an nd d M Me et t --h ho od ds s: : In this study, rats we re tre a ted with SrB and L-NNA 5-8 we eks af ter the in duc ti on of di a be tes. The le vels of glu tat hi o ne pe ro xi da se (GPx), su pe ro xi de dis mu ta se (SOD), ca ta la se (CAT) and ma lon di al dehy de (MDA) were de ter mi ned in the li ver ho mo ge na te and eryt hrocy te he moly sa te. The nit ric oxi de syntha se (NOS) le vels were al so me a su red in the li ver ho mo ge na te and se rum. To study the his to lo gi cal chan ges in di a be tes, the li ver tis su e samp les sta i ned with he ma toxy lein-eo sin and we re in ves ti ga ted under light mic ros co pe. R Re e s su ul lt ts s: : Alt ho ugh fas ting and post pran di al blo od su gar le vels we re high in di a be tic gro ups, blo od su gar le vels we re sig ni fi cantly re duced in di a be tic tre a ted gro ups. Whi le the erythrocyte MDA le vels of ste vi a-tre a ted di a be tic gro up dec re a sed, li pid pe ro xi da ti on in cre a sed with L-NNA tre at ment in both con trol and di a be tic gro ups. The re was no sig ni fi cant diffe ren ce for the tis su e CAT, NOS, and eryt hrocy te SOD and CAT ac ti vi ti es between. Li ver samp les in con trol group had a nor mal struc tu re. Nor mal his to lo gi cal ar ran ge ment was no ti ced in the li vers of con trol gro up. In he pa tocy tes of the di a be tic con trol gro up, nec ro tic cells with pycno tic nuc le us and eo si noph ylic cytop lasm as well as si nu so i dal di la ta ti on were se en. The he pa tocy te struc tu re was mo re pro tec ted in di a be tic LNNA gro up than in di a be tic gro up. The ma xi mum pro tec ti on was se en in he pa tocy tes of di a be tic ste vi a L-NNA gro up. C Co on nc c l lu u s si i --o on n: : SrB and L-NNA re du ced blo od glu co se le vels in di a be tic rats and had so me be ne fi ci al ef fects on oxi da ti ve and his to lo gi cal chan ges. Ho we ver, a NOS in hi bi tor, L-NNA was less ef fec ti ve than SrB tre at ment in type II di a betes.K Ke ey y W Wo or rd ds s: : Di a be tes mel li tus, type 2; ste vi a; nit ro ar gi ni ne; nit ric oxi de syntha se; fre e ra di cals Ö ÖZ ZE ET T A Am ma aç ç: : Ser best ra di kal üre ti mi di ya bet pa to ge ne zin de rol oy nar, bu ne den le ser best ra di kal ler di ya bet kompli kas yon la rı nın çe şit li yol la rı ve fark lı me ka niz ma la rın pa to fiz yo lo ji sin de et ki l...

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“…6,8,9 Both oxidative stress and inflammatory responses act as damaging agents in aggravating the pathological condition of DM. 4,10 In some cases, DM causes excessive accumulation of fat cells in the liver resulting in a fatty liver and, consequently, NAFLD. Subsequently, 2-3% of NAFLD patients experience hepatic inflammation, necrosis and fibrosis, which are symptoms of a condition known as non-alcoholic steatohepatitis (NASH).…”

mentioning

confidence: 99%

“…2 Research indicates that DM is associated with a number of liver abnormalities, such as abnormal glycogen deposition, non-alcoholic fatty liver disease (NAFLD), fibrosis, cirrhosis, hepatocellular carcinomas (HCCs), abnormal elevated hepatic enzymes, acute liver disease and viral hepatitis. 3,4 Additionally, an excessive accumulation of fat in the liver may worsen insulin resistance and lead to severe metabolic dysfunction. A fatty liver and hyperglycaemia can destroy the hepatocytes and contribute to increased morbidity and mortality among diabetic patients.…”

mentioning

confidence: 99%

Mechanisms of Diabetes-Induced Liver Damage: The role of oxidative stress and inflammation

Mohamed¹,

Nafizah²,

Zariyantey³

et al. 2016

SQUMJ

349

199

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Diabetes mellitus is a non-communicable disease that occurs in both developed and developing countries. This metabolic disease affects all systems in the body, including the liver. Hyperglycaemia, mainly caused by insulin resistance, affects the metabolism of lipids, carbohydrates and proteins and can lead to nonalcoholic fatty liver disease, which can further progress to non-alcoholic steatohepatitis, cirrhosis and, finally, hepatocellular carcinomas. The underlying mechanism of diabetes that contributes to liver damage is the combination of increased oxidative stress and an aberrant inflammatory response; this activates the transcription of pro-apoptotic genes and damages hepatocytes. Significant involvement of pro-inflammatory cytokinesincluding interleukin (IL)-1β, IL-6 and tumour necrosis factor-α-exacerbates the accumulation of oxidative damage products in the liver, such as malondialdehyde, fluorescent pigments and conjugated dienes. This review summarises the biochemical, histological and macromolecular changes that contribute to oxidative liver damage among diabetic individuals.

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Effects of melatonin on streptozotocin-induced diabetic liver injury in rats

Cited by 89 publications

References 33 publications

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

Antioxidant and Free Radical-Scavenging Properties of Stevia rebaudiana (Bertoni) Extracts and L-NNA in Streptozotocine-Nicotinamide Induced Diabetic Rat Liver

Mechanisms of Diabetes-Induced Liver Damage: The role of oxidative stress and inflammation

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