The effects of melatonin on brain nitrosative stress and energy balance in fructose-mediated metabolic syndrome model / Fruktoz-aracılı metabolik sendrom modelinde melatoninin beyinde nitrozatif stres ve enerji dengesi üzerine etkisi

2016 ◽  
Vol 41 (1) ◽  
Author(s):  
Gonca Ozan ◽  
Filiz Sezen Bircan ◽  
Turgut Topal ◽  
Nurten Türközkan
Keyword(s):  
Nitric Oxide ◽  
Metabolic Syndrome ◽  
Nitrosative Stress ◽  
Tap Water ◽  
Serum Triglyceride ◽  
Experimental Period ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Male Adult

AbstractObjective: Metabolic syndrome (MetS), one of the common health problems seen with increasing frequency in today’s modern societies, is also a important risk factor for neurological disorders such as stroke, depression, Alzheimer’s disease. On the other hand, melatonin is a neurohormone, has potent antioxidant and neuroprotective activities. In the present study, we aimed to investigate the possible protective effects of melatonin administration on brain tissue in fructose-mediated MetS model.Methods: Male adult Sprague-Dawley rats were randomly divided into four groups (n=8); control, fructose, melatonin and fructose plus melatonin. MetS was induced by fructose solution 20% in tap water, and melatonin was administered at the dose of 20 mg/kg bw/day by oral gavage. Systolic blood pressures (SBP) were measured by tail-cuff method. After the experimental period of 8 weeks, serum triglyceride, glucose, insulin, and tissue ATP/ADP ratio, nitric oxide (NOx) and 3-nitrotyrosine (3-NT) levels were measured. Also tissue endothelial and inducible nitric oxide synthase (eNOS and iNOS) protein levels were determined.Results: Fructose consumption increased SBP, serum triglyceride, insulin levels and induced insulin resistance significantly compared to control group and MetS model was successfully demonstrated. In comparison with control group, fructose administration did not cause significant changes in tissue ATP/ADP ratio and 3-NT levels. NOx levels did not change significantly among groups, and iNOS-eNOS proteins were not detected in any groups. Interestingly, tissue 3-NT levels were elevated significantly while ATP/ADP ratio was diminished in fructose plus melatonin group compare with both control and fructose groups.Conclusion: These results indicate that high fructose diet for 8 weeks does not influence nitric oxide production, energy metabolism and protein nitration in brain. Nevertheless melatonin acted as a pro-oxidant at that dose when administered with fructose.

Protective effects of telmisartan and tempol on lipopolysaccharide-induced cognitive impairment, neuroinflammation, and amyloidogenesis: possible role of brain-derived neurotrophic factor

2017 ◽  
Vol 95 (7) ◽  
pp. 850-860 ◽  
Author(s):  
Waleed A.I. Khallaf ◽  
Basim A.S. Messiha ◽  
Amira M.H. Abo-Youssef ◽  
Nesrine S. El-Sayed
Keyword(s):  
Nitric Oxide ◽  
Cognitive Impairment ◽  
Angiotensin Ii ◽  
Nitrosative Stress ◽  
Histopathological Examination ◽  
Control Group ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Brain Levels ◽  
Tnf Α

Angiotensin II has pro-inflammatory and pro-oxidant potentials. We investigated the possible protective effects of the Angiotensin II receptor blocker telmisartan, compared with the superoxide scavenger tempol, on lipopolysaccharide (LPS)-induced cognitive decline and amyloidogenesis. Briefly, mice were allocated into a normal control group, an LPS control group, a tempol treatment group, and 2 telmisartan treatment groups. A behavioral study was conducted followed by a biochemical study via assessment of brain levels of beta amyloid (Aβ) and brain-derived neurotropic factor (BDNF) as amyloidogenesis and neuroplasticity markers, tumor necrosis factor alpha (TNF-α), nitric oxide end products (NOx), neuronal and inducible nitric oxide synthase (nNOS and iNOS) as inflammatory markers, and superoxide dismutase (SOD), malondialdehyde (MDA), glutathione reduced (GSH), and nitrotyrosine (NT) as oxido-nitrosative stress markers. Finally, histopathological examination of cerebral cortex, hippocampus, and cerebellum sections was performed using routine and special Congo red stains. Tempol and telmisartan improved cognition, decreased brain Aβ deposition and BDNF depletion, decreased TNF-α, NOx, nNOS, iNOS, MDA, and NT brain levels, and increased brain SOD and GSH contents, parallel to confirmatory histopathological evidences. In conclusion, tempol and telmisartan are promising drugs in managing cognitive impairment and amyloidogenesis, at least via upregulation of BDNF with inhibition of neuroinflammation and oxido-nitrosative stress.

scholarly journals Pistacia Terebinthus Coffee Protects against Thioacetamide-Induced Liver Injury in Rats

2015 ◽  
Vol 58 (2) ◽  
pp. 56-61 ◽  
Author(s):  
Ibrahim Halil Bahçecıoğlu ◽  
Murat Ispiroglu ◽  
Mehmet Tuzcu ◽  
Cemal Orhan ◽  
Mustafa Ulas ◽  
...  
Keyword(s):  
Liver Injury ◽  
Transforming Growth Factor Beta ◽  
Unsaturated Fatty Acids ◽  
Transforming Growth Factor ◽  
Tap Water ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Pistacia Terebinthus

Aim/background: Pistacia terebinthus is used as a coffee substitute in the East and Southern Anatolia regions of Turkey. It contains unsaturated fatty acids, tocopherols, polyphenols and carotenoids. P. terebinthus has anti-inflammatory and potential antioxidant activity. In this study we evaluated the protective effects of P. terebinthus coffee (PTC) on thioacetamide (TAA)-induced liver injury in rats. Materials and methods: Twenty-eight male Sprague-Dawley rats were equally randomized into four groups. Chronic liver injury was induced with TAA (100 mg/kg i.p. three times weekly). The first group of rats served as control and received only tap water (G1), and the remaining groups of rats received PTC, p.o (G2); TAA (G3); TAA plus PTC, p.o (G4), respectively. Results: After 8 weeks, PTC intake significantly reduced fibrosis/inflammation scores (p < 0.05) in the livers of TAA-treated group. Compared to control group, PTC intake reduced transforming growth factor beta (TGF-β) concentrations in the liver (p < 0.05). Compared to the TAA group, TGF-β, nuclear factor kappa B (NF)-κB (p < 0.05), tumor necrosis factor alpha (TNF-α) concentrations in the liver tissue were reduced by PTC intake. Discussion and conclusion: PTC intake provided beneficial effects against TAA-induced liver injury in rats. PTC probably suppresses the proinflammatory cytokines through NF-κB signaling pathway.

scholarly journals Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1407 ◽  
Author(s):  
You-Lin Tain ◽  
Julie Chan ◽  
Chien-Te Lee ◽  
Chien-Ning Hsu
Keyword(s):  
Methylation Status ◽  
Normal Diet ◽  
Male Offspring ◽  
Adult Offspring ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Male Adult ◽  
Methyl Donor ◽  
Adult Rat

Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or a high methyl-donor diet (H-MD) during gestation and lactation. Male offspring were assigned to four groups (n = 7–8/group): control, L-MD, H-MD, and H-MD rats were given melatonin (100 mg/L) with their drinking water throughout the period of pregnancy and lactation (H-MD+M). At 12 weeks of age, male offspring exposed to a L-MD or a H-MD diet developed programmed hypertension. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. A maternal L-MD diet and H-MD diet caused respectively 938 and 806 renal transcripts to be modified in adult offspring. The protective effects of melatonin against programmed hypertension relate to reduced oxidative stress, increased urinary NO2− level, and reduced renal expression of sodium transporters. A H-MD or L-MD diet may upset the balance of methylation status, leading to alterations of renal transcriptome and programmed hypertension. A better understanding of reprogramming effects of melatonin might aid in developing a therapeutic strategy for the prevention of hypertension in adult offspring exposed to an excessive maternal methyl-supplemented diet.

scholarly journals Effect of a Lower Limb Restless Period on Expression of Mir-1 and Mir-206 Neural Muscle Genes in Endurance Training Rats

2020 ◽  
Vol 23 (4) ◽  
pp. 570-579
Author(s):  
Mahboubeh Sheikhan ◽  
◽  
Mohammad Reza Kordi ◽  
Hamid Rajabi ◽  
◽  
...  
Keyword(s):  
Muscular Atrophy ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Medical Sciences ◽  
Sprague Dawley Rats ◽  
Muscle Genes ◽  
Univariate Anova ◽  
Pcr Method ◽  
Post Hoc

Background and Aim: Several microRNAs are involved in regulating muscle mass, which plays an essential role in hypertrophy and atrophy of skeletal muscle, The present study examined the expression of some genes as regulators of muscular atrophy following a period of inertia in rats. Methods & Materials: For this purpose, 18 male Sprague-Dawley rats were divided into three groups (Control, Exercise+inactivity, and Inactivity). The exercise+inactivity group run on the treadmill for 18 weeks and five times per week. The hindlimb of the animal was immobilized for seven days with the casting method. Soleus muscle was extracted and the expression of the genes was measured by the RT-PCR method. Univariate ANOVA and Tukey post hoc test was used to determine the differences (α=0.05). Ethical Considerations: The Ethics Committee of the Tehran University of Medical Sciences Research approved this study (Code: IR.SUMS.REC.1396.S 463). Results: Results showed that immobilization in both Exercise+ inactivity and inactivity groups, compare to the control group, increased expression of miR-1 genes (P<0.10), FOXO3a (P<0.001) and decreased expression of miR-206 (P<0.007) and IGF-1 (P<0.001). This difference was statistically significant. Conclusion: According to the results of this study, it can be said that changes in the expression of RNAs by chromatography cause changes in the expression of muscle regulating genes, and although endurance exercises have protective effects, they cannot prevent these changes.

Protective effects of dietary omega-3 fatty acid supplementation on organophosphate poisoning

2017 ◽  
Vol 34 (2) ◽  
pp. 69-82 ◽  
Author(s):  
Bahattin Avci ◽  
S. Sirri Bilge ◽  
Gokhan Arslan ◽  
Omer Alici ◽  
Ozge Darakci ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Olive Oil ◽  
The Body ◽  
Control Group ◽  
Organophosphate Poisoning ◽  
Protective Effects ◽  
Omega 3 ◽  
Sprague Dawley ◽  
Omega 3 Fatty Acid ◽  
Locomotor Activities

In this study, we aimed to study the possible preventive effect of docosahexaenoic acid (DHA), a dietary omega-3 fatty acid, on toxicity caused by chlorpyrifos (CPF). Six groups of Sprague Dawley rats (200–250 g) consisting of equal numbers of males and females (n = 8) were assigned to study. The rats were orally given for 5 days. The control group was administered pure olive oil, which was the vehicle for CPF. The CPF challenge groups were administered oral physiological saline, pure olive oil, or DHA (50, 100 and 400 mg/kg dosages) for 5 days. The animals were weighed on the sixth day and then administered CPF (279 mg/kg, subcutaneously). The rats were weighed again 24 h following CPF administration. The body temperatures and locomotor activities of the rats were also measured. Blood samples, brain and liver tissues were collected for biochemical, histopathological and immunohistochemical examinations. A comparison with the control group demonstrated that CPF administration increased malondialdehyde (MDA) levels in blood, brain and liver, while it reduced catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) concentrations ( p < 0.05–0.001). Advanced oxidation protein products (AOPPs) increased only in the brain ( p < 0.001). DHA reduced these changes in MDA and AOPP values ( p < 0.05–0.001), while it increased CAT, SOD and GPx concentrations ( p < 0.05–0.001). Similarly, DHA prevented the decreases in body weight, body temperature and locomotor activities caused by CPF at 100 mg/kg and 400 mg/kg dosages ( p < 0.05–0.001). Similar to the physiological and biochemical changes, the histopathological damage scores, which increased with CPF ( p < 0.05–0.01), decreased at all three dosages of DHA ( p < 0.05–0.01). Our findings suggest that DHA, by supporting the antioxidant mechanism, reduces toxicity caused by CPF.

Exosome derived from mesenchymal stem cells enhance autophagy and inhibit iNOS/TXNIP/NLRP3 inflammasome axis in injured spinal cord

2020 ◽  
Author(s):  
Bin Lv ◽  
Lei Wang ◽  
Anquan Huang ◽  
Tianming Zou ◽  
Jishan Yuan
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Nlrp3 Inflammasome ◽  
Neuroprotective Effect ◽  
Neuronal Cells ◽  
Tissue Loss ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Cord Injury

Abstract Background: Neuroinflammation, autophagy, NLRP3 inflammasome, and microglia polarizationhave been implicated in spinal cord injury (SCI).Moreover, exosomes, a classic nanovesicles secreted by MSCs, may have a neuroprotective effect on transformation of microglia from the M1 state to the M2 phenotype. However, the effect of MSCs derived exosomes on neuroinflammation is still unclear. Here, we investigated the mechanisms of MSCs derived exosomes mediated NLRP3 inflammasome signaling cascades and its protective effects in SCI. Methods:The SCI model was performed by weight-drop impact in adult male Sprague-Dawley (SD) rats. Control andexosome rats were randomly subjecttoexosomeadminister (20 mg/kg) or placebo via intraperitoneal route 1 h after SCI.Autophagy inhibitor(3-MA) was administered intraperitoneally 20 min before experiment.Neurological function was measured by Basso-Beattie-Bresnahan (BBB) scoring and an open-field test.Neuronal death was measured by HE stainingandNisslstaining.Inducible nitric oxide synthase (iNOS) levels were determined using fluorescent probes. The autophagy and TXNIP and its downstream signaling pathways-mediated polarization of macrophages/microglia was assessed by immunohistochemistry. Results:Exosome significantly downregulated intracellular iNOS and inhibited TXNIP, pyrin domain-containing 3 (NLRP3) inflammasome pathway activation by activating autophagy. Additionally, Exosomepromoted expression of autophagy markers, such as LC3A/B and beclin1,and abrogated the expression of p62. Autophagy inhibitor, 3-MA, blockage of autophagy flux abolished the inhibition of apoptosis and iNOS/TXNIP/NLRP3 inflammasome axisafterSCI. Here, we demonstrated that exosomeadministration in spinal cord markedly reduced tissue loss, attenuate pathological morphology of the injuredregion, and promoted tissue recovery. Moreover. our resultshowed that exosome administration alleviated neuronal cells apoptosis, and inhibited nitric oxide release in microglia.The activation of inflammatoryresponse in neuronal cells facilitates interactions of iNOS‐NLRP3 andTXNIP‐NLRP3and inhibited NLRP3 inflammasome where neuronal cells apoptosis was induced.Further, we found that exosome could suppress macrophages/microglia polarized to M1 phenotype in vivo and in vitro.Taken together, exosome administration exerts protective effects in neuronal cells through inhibiting iNOS production, and exosome administration could inhibit iNOS/TXNIP/NLRP3 inflammasome axis via enhancing autophagy and both in vitro and in vivo. Conclusions:These resultsreveal that exosometreatment alleviatedneuroinflammation and mitigates neuronal apoptosis via autophagy-mediate inhibition of the iNOS/TXNIP/NLRP3 inflammasome axis. Our findings suggest that exosome may be a novel therapeutic target for treating SCI.

Effects of probiotics-encapsulated live feed on growth and survival of juvenile Clarias batrachus (Linnaeus, 1758) after differential exposure to pathogenic bacteria

2018 ◽  
Vol 16 (1) ◽  
pp. 105-113 ◽  
Author(s):  
A Dey ◽  
K Ghosh ◽  
N Hazra
Keyword(s):  
Pathogenic Bacteria ◽  
Experimental Period ◽  
Clarias Batrachus ◽  
Control Group ◽  
Continuous Exposure ◽  
Protective Effects ◽  
Growth And Survival ◽  
Treatment Groups ◽  
Live Feed ◽  
Differential Exposure

Growth and survival of Clarias batrachus juveniles (10-day old) fed probiotic Bacillus cereus (KR809412) encapsulated live feed (chironomid larvae) have been evaluated after differential exposure to the pathogenic Aeromonas hydrophila (MTCC 1739). Catfish juveniles were stocked at a density of 30 fish per tank in five experimental groups (T1-T5) along with a control group in triplicate and fed twice @ 5% of body weight day-1 for four weeks. Groups T1 and T2 were fed probiotic-encapsulated (PR) or pathogen-inoculated (PGN) live feed respectively, for initial three weeks. During this period groups T3 (PGN-PR-PR), T4 (PR-PGN-PR), and T5 (PR-PR-PGN) were differentially exposed to the pathogen. Live feed without probiotic and pathogen was offered to the control group throughout the experimental period and all other treatment groups (T1-T5) during the 4th week. Continuous exposure to probiotics in group T1 resulted in significantly higher (P<0.05) specific growth rate (SGR, % d-1) and survivability than other groups, whereas, pathogen exposed and probiotic deprived group (T2) noticed with the lowest SGR and the highest mortality. Among other treatment groups (T3, T4 and T5), group T4 resulted in improved SGR and survivability. The coefficient (r value) of 0.867 along with regression slope suggested a positive correlation (0.01 levels) between RNA: DNA and SGR. The study might suggest protective effects of probiotic B. cereus in pathogen exposed C. batrachus juveniles.SAARC J. Agri., 16(1): 105-113 (2018)

P1572EFFECTIVENESS OF COENZYME Q10-MICELLE COMPARED WITH COENZYME Q10 ON TACROLIMUS-INDUCED RENAL INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sheng Cui ◽  
Kang Luo ◽  
Yi Quan ◽  
Sun Woo Lim ◽  
Chul-Woo Yang
Keyword(s):  
Oxidative Stress ◽  
Coenzyme Q10 ◽  
Renal Injury ◽  
Apoptotic Cell ◽  
Oxidative Stress Marker ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Male Adult ◽  
Sprague Dawley Rats ◽  
Pathologic Lesions

Abstract Background and Aims We and others have recently demonstrated that Coenzyme Q10 (CoQ10) has protective effects against diabetes mellitus and various types of renal injury. This study investigated whether CoQ10-micelle treatment would affords superior renoprotection compared with CoQ10 in the governing tacrolimus (Tacrolimus)-induced renal injury in the rats. Method Male adult Sprague-dawley Rats were treated daily with Tacrolimus (1.5mg/kg/day, subcutaneous), CoQ10 (20mg/kg/day, oral), and CoQ10-micelle (20 mg/kg/day, oral) for 4 weeks. The effects of CoQ10 orCoQ10-micelle on Tac-induced renal injury were assessed in terms of renal function, histopathology, oxidative stress and apoptotic cell death. Results After 4 weeks of Tacrolimus treatment to rats caused renal dysfunction, typical pathologic lesions, and oxidative stress marker. The serum creatinine was reduced by Tac co-treatment with CoQ10 or CoQ10-micelle groups compared with the Tac and VH group (0.31 ± 0.03 in the VH group vs. 0.43 ± 0.041 in the Tac group vs.0.37 ± 0.031 in the Tac+CoQ10 group 0.30 ± 0.02123 in the Tac+CoQ10-micellegroup; 1P&lt;0.05 vs. VH. 2P&lt;0.05 vs. TAC. . 3P&lt;0.05 vs. TAC+C.) The administration of CoQ10-micelle improved renal immunoreactivity, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that tacrolimus co-treatment with CoQ10-micelle increased the size and number of mitochondria more than co-treatment with CoQ10, compared with that induced by TAC treatment alone. Conclusion These findings suggest that both CoQ10 and CoQ10-micelle effectively attenuates Tac-induced renal injury, and CoQ10-micelle provides more benefits than that of CoQ10.

scholarly journals Relevance of a Hypersaline Sodium-Rich Naturally Sparkling Mineral Water to the Protection against Metabolic Syndrome Induction in Fructose-Fed Sprague-Dawley Rats: A Biochemical, Metabolic, and Redox Approach

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Cidália Dionísio Pereira ◽  
Milton Severo ◽  
João Ricardo Araújo ◽  
João Tiago Guimarães ◽  
Diogo Pestana ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Mineral Water ◽  
Tap Water ◽  
Magnesium Content ◽  
Atherosclerotic Cardiovascular Disease ◽  
Sprague Dawley ◽  
The Metabolic Syndrome ◽  
Sprague Dawley Rats ◽  
Calcium And Magnesium

The Metabolic Syndrome increases the risk for atherosclerotic cardiovascular disease and type 2 Diabetes Mellitus. Increased fructose consumption and/or mineral deficiency have been associated with Metabolic Syndrome development. This study aimed to investigate the effects of 8 weeks consumption of a hypersaline sodium-rich naturally sparkling mineral water on 10% fructose-fed Sprague-Dawley rats (Metabolic Syndrome animal model). The ingestion of the mineral water (rich in sodium bicarbonate and with higher potassium, calcium, and magnesium content than the tap water used as control) reduced/prevented not only the fructose-induced increase of heart rate, plasma triacylglycerols, insulin and leptin levels, hepatic catalase activity, and organ weight to body weight ratios (for liver and both kidneys) but also the decrease of hepatic glutathione peroxidase activity and oxidized glutathione content. This mineral-rich water seems to have potential to prevent Metabolic Syndrome induction by fructose. We hypothesize that its regular intake in the context of modern diets, which have a general acidic character interfering with mineral homeostasis and are poor in micronutrients, namely potassium, calcium, and magnesium, could add surplus value and attenuate imbalances, thus contributing to metabolic and redox health and, consequently, decreasing the risk for atherosclerotic cardiovascular disease.

scholarly journals Sulodexide Protects Contrast-Induced Nephropathy in Sprague-Dawley Rats

2016 ◽  
Vol 40 (3-4) ◽  
pp. 621-632 ◽  
Author(s):  
Qing Zhao ◽  
Jianyong Yin ◽  
Zeyuan Lu ◽  
Yiwei Kong ◽  
Guangyuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Vehicle Group ◽  
Control Group ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Contrast Induced Nephropathy ◽  
Sprague Dawley Rats ◽  
Hk2 Cells

Background: Sulodexide is a powerful antithrombin agent with reno-protective property. However, whether it has beneficial effects on Contrast-Induced Nephropathy (CIN) remained elusive. In the current study, we evaluated the therapeutic effects of Sulodexide on CIN and investigated the potential mechanisms. Methods: CIN model was induced by intravenous injection of indomethacin, followed by Ioversol and L-NAME. Sprague-Dawley rats were divided into 4 groups: control group, CIN group, CIN+vehicle group (CIN rats pretreated with vehicle) and CIN+ Sulodexide (CIN rats pretreated with Sulodexide). Sulodexide or an equivalent volume of vehicle was intravenously delivered 30 min before the induction of CIN. All the animals were sacrificed at 24h after CIN and tissues were harvested to evaluate renal injury, kidney oxidative stress and apoptosis levels. Plasma antithrombin III (ATIII) activities were also measured. Results: Compared to the untreated CIN group, improved renal function, reduced tubular injury, decreased levels of oxidative stress and apoptosis were observed in CIN rats receiving Sulodexide injection. In addition, we also found that ATIII activity was significantly higher in Sulodexide-administered group than that in vehicle-injected CIN rats. For in vitro studies, HK2 cells were exposed to Ioversol and the cyto-protective effects of Sulodexide were also determined. Sulodexide pretreatment protected HK2 cells against the cytotoxicity of Ioversol via inhibiting caspase-3 activity. Preincubation with Sulodexide could also attenuate H2O2-induced increases in ROS, apoptosis and caspase-3 levels. Conclusions: Taken together, Sulodexide could protect against CIN through activating ATIII, and inhibiting oxidative stress, inflammation and apoptosis.

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