The Antioxidant Activity of Pistachios Reduces Cardiac Tissue Injury of Acute Ischemia/Reperfusion (I/R) in Diabetic Streptozotocin (STZ)-Induced Hyperglycaemic Rats
Rosanna Di PaolaRoberta FuscoEnrico GugliandoloRamona D’AmicoMichela CampoloSaverio LatteriArianna CarughiGiuseppina MandalariSalvatore Cuzzocrea
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Abstract:
Diabetes mellitus is an important risk factor for the development of heart pathology. Myocardial infarction is the cause of death occurring after prolonged ischemia of the coronary arteries. Restoration of blood flow is the first intervention against heart attack, although the process of restoring blood flow to the ischemic myocardium could cause additional injury. This phenomenon, termed myocardial ischemia-reperfusion (MI-R) injury, is characterized by the formation of oxygen radicals. Pistachios have significant glucose- and insulin-lowering effects and can improve the inflammatory contest by downregulating both the expression and the circulating levels of several metabolic risk markers. The monocyte/macrophage cell line J774 was used to assess the extent of protection by natural raw (NP) and roasted salted (RP) pistachios against lipopolysaccharide (LPS)-induced inflammation. Moreover, antioxidant activity of NP and RP was assessed in an in vivo model of paw edema in rats induced by carrageenan (CAR) injection in the paw. This study evaluates the antioxidant properties of pistachios on the inflammatory process associated with myocardial ischemia/reperfusion injury (I/R) in diabetic rats. Rats were pre-treated with either NP or RP pistachios (30 mg/kg) 18 h prior to the experimental procedure. Results: Here, we demonstrated that treatment with NP reduced myocardial tissue injury, neutrophil infiltration, adhesion molecules (ICAM-1, P-selectin) expression, proinflammatory cytokines (TNF-α, IL-1β) production, nitrotyrosine and PAR formation, NF-κB expression and apoptosis (Bax, Bcl-2) activation. This data clearly showes modulation of the inflammatory process, associated with MI-R injury, following administration of pistachios.Keywords:
Proinflammatory cytokine
Nitrotyrosine
Hypoxia
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Ischemia is defined as cell death caused by insufficient perfusion of the tissue due to reduction in arterial or venous blood flow, depletion of cellular energy storages, and accumulation of toxic metabolites. The positive effects of controlled reperfusion are known and are used clinically. But the positive effects of controlled reperfusion on ovarian tissue have not been seen in the literature yet. The biochemical and histopathological comparative investigation of rat ovaries that were experimentally exposed to ischemia (IG), ischemia-reperfusion (I/R), and ischemia-controlled reperfusion (ICR) was aimed. Forty rats were divided into four groups (10 rats per group). First group: 3 h ischemia by vascular clips on ovarian tissue. Second group: 3 h ischemia + 1 h reperfusion. Third group: 3 h ischemia + 1 h controlled reperfusion (on-off method: controlled reperfusion by opening and closing the clips (on/off) in 10-second intervals, for 5 times for a total of 100 seconds). Fourth group: healthy rats. Biochemical (tGSH, MDA, and DNA damage level and SOD activity) and histopathological analysis were performed. The highest glutathione and superoxide dismutase measurements were found in ischemia/controlled reperfusion group among the ischemia or ischemia/reperfusion groups. Similarly the damage indicators (malondialdehyde, DNA damage level and histopathological damage grade) were the lowest in ischemia/controlled reperfusion group. These results indicate that controlled reperfusion can be helpful in minimizing ischemia-reperfusion injury in ovarian tissue exposed to ischemia for various reasons (ovarian torsion, tumor, etc.).
Ovarian torsion
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Altered nitric oxide (NO) metabolism has been shown to contribute to ischemia-reperfusion (IR) injury in animal models. However, similar studies have not been performed in human liver transplantation (LT). In this study, we examined nitrate, nitrite, and nitrosothiols (NOx), NO synthases (endothelial [constitutive] nitric oxide synthase [eNOS] and inducible nitric oxide synthase [iNOS]), and nitrotyrosine in early IR injury after human LT.Paired biopsies were obtained from nine donor livers before cold ischemia (retrieval biopsy) and after reimplantation (reperfusion biopsy). Sections were graded for reperfusion injury using the Suzuki score. NO was detected by chemiluminescence after reduction of NOx. Expression of eNOS and iNOS was by Western blot and reverse transcriptase polymerase chain reaction and peroxynitrite by immunodetection of 3-nitrotyrosine.Reperfusion biopsies showed histologic evidence of injury (median Suzuki score: retrieval 2, reperfusion 6, P=0.008) and neutrophil infiltration. NOx was reduced after reperfusion from 5.41 microM/100 mg (median, range 2.17-13.39 microM) to 3.51 microM (1.45-5.66 microM, P=0.05). eNOS protein was reduced after reperfusion from 0.6 units (median, range 0.45-1 unit) in retrieval biopsies to 0.39 units in reperfusion biopsies (range 0.2-0.79 units, P=0.007). There was no change in eNOS or iNOS mRNA expression or iNOS protein. Western blotting showed increased nitrotyrosine formation after reperfusion, median 0.42 (range 0.16-0.87) units in retrieval biopsies and 0.68 (0.29-1.06) units in reperfusion samples (P=0.007) and localized to periportal regions.iNOS protein may not contribute to early reperfusion injury during human LT. However, reduced NO bioavailability caused by reduced eNOS may contribute significantly to damage at this time point.
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Objective: To study NF-κB and IL-6 expression in a rat retina that has been inj ured by ischemia-reperfusion and the effect of β-aescin on its expression.Methods: A retinal model of the rat retina for ischemia-reperfusion was establi s hed. 60 SD rats were divided into two groups: one was an ischemia-reperfusion g r oup and the other was an ischemia-reperfussion and β-aescin group. Each group wa s then divided into sub-groups according to the amount of time after ischemia- re perfusion:1 hour,6 hours,12 hours,24 hours,48 hours,and 72 hours. Each sub -group consisted of 5 rats. NF-κB mRNA and IL-6 mRNA in the rat retina was m easured by the ISH method. Each rat was examined by ERG before being sacrificed.Results: NF-κB and IL-6 began to express at 6 hours after ischemia-reperfusio n i n the ischemia-reperfusion group. The highest level of expression occurred 24 h o urs after injury. In the ischemia-reperfusion and β-aescin group,the NF-κB and IL-6 expressed at 12 hours after ischemia-reperfusion injury and reached the hi ghest level at 24 hours. However,its level was lower than the level for the isc hemia-reperfusion group at every stage(P0.05). The b wave of the ERG in the is chemia-reperfusion group was lower than that for the ischemia-reperfusion and β-aescin group at every stage(P0.05).Conclusion: NF-κB may induce IL-6 and play an important role in ischemia-reperfusion inj ury in the rat retina. The β-aescin may suppress NF-κB activity and protect the retina from injury caused by ischemia-reperfusion.
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Abstract Objectives The study was to explore the influence of microRNA (miR)-345-3p on proinflammatory cytokines in patients with rheumatoid arthritis (RA). Methods A total of 32 RA patients and 32 healthy patients were enrolled. Proinflammatory factors in patients’ serum were detected by ELISA, and miR-345-3p was detected by RT-qPCR. The correlation between miR-345-3p expression and proinflammatory factors in RA patients was analyzed. The diagnostic value of miR-345-3p and proinflammatory factors in RA patients was analyzed by receiver operating curve diagnosis. The predictive value of miR-345-3p levels and proinflammatory factors in RA patients was analyzed by multivariate Cox regression. HFLS-RA and HFLS cells were cultured, in which miR-345-3p and proinflammatory cytokines were detected by RT-qPCR. Cell proliferation and apoptosis were determined by CCK-8 and flow cytometry, respectively. Results MiR-345-3p was lowly expressed in the serum of RA patients. MiR-345-3p and proinflammatory factors were of diagnostic and predictive values in RA. Elevated miR-345-3p restrained the production of proinflammatory factors of HFLS-RA cells, improved cell proliferation, and reduced apoptosis. Conclusion MiR-345-3p is a potential biomarker and ameliorates RA by reducing the release of proinflammatory cytokines.
Proinflammatory cytokine
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[Objective]To study the IL-6 express in rat's retina which injuried by ischemia-reperfusion and the effect of β-aescin on its expression. The model of rat's retina ischemia-reperfusion was employed. 60 SD rats were devided into two groups, one was ischemia-reperfusion group, the other was ischemia-reperfusion andβ-aescin group. Every group was devided into 1 hour, 6 hour, 12 hour, 24 hour, 48 hour and 72 hour groups. Every group had 5 rats. IL-6 mRNA was measured by ISH method in rat's retina. Every rat was examinated ERG before executed. IL-6 began to express at 6 hours after ischemia-reperfusion in ischemia-reperfusion group. It expressed most at 24 hours after ischemia-reperfusion injury. In ischemia-reperfusion and β-aescin group, IL-6 expressed at 12 hours after ischmia-reperfusion injury and reached the hightest level was lower than ischemia-reperfusion group at every stage (P 0.05). The a wave of ERG of ischemia-reperfusion group was lower than ischemia-reperfusion and β-aescin group at every stage (P 0.05). [Conclusion] IL-6 take important role in rat's retina ischemia-reperfusion injury, the β-aescni may suppress the activity of IL-6 and relieve the retina injury from the ischemia-reperfusion.
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Objective To investigate the effect of palm oil(PO) on the volume of the infarction,the expression of Bcl-2 and Bax protein following focal cerebral ischemia/reperfusion in rats,and explore the protective effect of PO on focal cerebral ischemia/reperfusion and the underlying mechanism.Methods The acute focal cerebral ischemia/reperfusion models were established with suture emboli.Healthy male Sprague-Dawley rats were randomly divided into four groups: normal control group,sham group,IR group and PO group.There were 12 rats in each of the normal control group and the sham group.The IR group and PO group were further subdivided into subgroups and sacrificed 2 h,6 h,12 h,24 h,72 h and 7 d after ischemia/reperfusion(n=12).The volume of the infarction was observed by the TTC method;and the expression of Bcl-2 and Bax was determined by Western blotting to observe the protective effect of PO.Results ① TTC staining: there was no region of ischemia/reperfusion injury in the normal control group and the sham group.There was no region of ischemia/reperfusion injury in IR group and PO group 2 h after ischemia/reperfusion.At the time points of 6 h,12 h,24 h,72 h and 7 d after ischemia/reperfusion,there were statistical differences in mass percentage of the infracted regions between the PO group and the IR group(P0.05),and mass percentage of the infracted cerebral regions in the PO group was reduced as compared to the IR group.② Western-blotting: From the time point of 6h after reperfusion,in both PO group and IR group,the expression of Bcl-2 and Bax increased with time in the ischemia penumbra with peak expression at 12 h,and then decreased.The expression of Bax reached the peak at 24 h,and then decreased.Western-blotting analysis showed a gradual increase in Bcl-2 expression(P0.05) and a gradual decrease in Bax expression(P0.05) in PO group at each time point(6 h,12 h,24 h and 72 h after ischemia/reperfusion),compared with IR group.Conclusions ① PO can reduce the region of ischemia injury following focal cerebral ischemia/reperfusion injury;② PO can protect nerve cells by increasing the expression of Bcl-2 and decreasing the expression of Bax,following the cerebral ischemia/reperfusion injury.
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Objective To investigate the changes in iNOS expression in brain injury induced by hepatic ischemia-reperfusion (IR) in rats.Methods Thirty-two male Wistar rats weighing 240-280 g were randomly divided into 2 groups: sham operation group (group S,n = 8) and group IB( n = 24).The hepatic IR was induced by clamping the hepatic artery and portal vein according te the method described by LONG et al.In group IR the rats were killed at 3,6 and 24 h of reperfusion after 40 min hepatic ischemia (8 rats at each time point).The rats in group S were also killed.The brains were removed for determination of NO content (by nitrate reductase assay),SOD activity (by xanthine oxidase method),MDA content(by colorimetric method),nitrotyrosine (NT) expression (by Western blot),and iNOS mRNA expression (by RT-PCR).Results Compared with group S,cerebral NO and MDA content were significantly increased at 6 and 24 h of reperfusion,expression of cerebral NT and iNOS mRNA up-regulated and SOD activity decreased at 6 h of reperfusion in group IR (P < 0.05 or 0.01).Cerebral NO and MDA content were significantly higher and SOD activity lower at 6 and 24 h of reperfusion than at 3 h of reperfusion in group IR (P < 0.05).Conclusion The expression of iNOS in brain tissues is up-regulated after hepatic IR and it produces a great amount of NO inducing brain injury through peroxynitrite (ONOO-).
Key words:
Nitric-oxide synthase; Brain injuries; Liver; Reperfusion injury
Nitrotyrosine
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Nitrotyrosine
Ischemic Preconditioning
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