The protective effects of dexmedetomidine against apoptosis in retinal ischemia/reperfusion injury in rats

Gencer, Baran; Karaca, Turan; Tufan, Hasan Ali; Kara, Selçuk; Arıkan, Sedat; Toman, Hüseyin; Karaboğa, İhsan; Hancı, Volkan

doi:10.3109/15569527.2013.857677

Cited by 17 publications

(12 citation statements)

References 32 publications

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“…Light microscopic investigation of renal histology and scoring of damage were conducted as described before [18, 28, 33, 34]. Briefly, the kidney (4 μm sections) were cut and stained with hematoxylin (H & E), Masson Trichrome and Sirius Red stain.…”

Section: Methodsmentioning

confidence: 99%

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The effect of swimming exercise on adenine-induced kidney disease in rats, and the influence of curcumin or lisinopril thereon

et al. 2017

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Patients with chronic kidney disease (CKD) have been reported to benefit from different types of exercises. It has also been shown that the ACE inhibitor lisinopril, and the natural product curcumin are also beneficial in different models of CKD in rats. We assessed the influence of moderate swimming exercise (SE) on rats with adenine-induced CKD, and tested the possible effects of lisinopril and/or curcumin thereon using several physiological, biochemical, histopathological and immunohistochemical parameters. Rats (either sedentary or subjected to SE) were randomly divided into several groups, and given for five weeks either normal food or food mixed with adenine (0.25% w/w) to induce CKD. Some of these groups were also concomitantly treated orally with curcumin (75 mg/kg), or lisinopril (10 mg/kg) and were subjected to moderate SE (45 min/day three days each week). Rats fed adenine showed the typical biochemical, histopathological signs of CKD such as elevations in blood pressure, urinary albumin / creatinine ratio, and plasma urea, creatinine, indoxyl sulfate and phosphorus. SE, curcumin or lisinopril, given singly, significantly ameliorated all the adenine-induced actions. Administering curcumin or lisinopril with SE improved the histopathology of the kidneys, a salutary effect not seen with SE alone. Combining SE to the nephroprotective agents’ curcumin or lisinopril might offer additional nephroprotection.

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Section: Methodsmentioning

confidence: 99%

“…2.11.5.1, Istanbul, Turkey). All the counts were converted to number of positive cells per unit area (mm 2 ) [33, 34]. …”

Section: Methodsmentioning

confidence: 99%

The effect of swimming exercise on adenine-induced kidney disease in rats, and the influence of curcumin or lisinopril thereon

et al. 2017

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“…In addition, some studies have reported that DEX preconditioning effectively reduces the inflammatory response of myocardial, renal and spinal cord ischemia by downregulation of high-mobility group protein B1 (HMGB1)/toll-like receptor 4 (TLR4) pathways (Gu et al, 2011; Rong et al, 2017; Yang et al, 2017). Meanwhile, DEX has been reported being protective in brain, intestinal, renal and lung by inhibiting apoptosis, necrosis (Engelhard et al, 2003; Gencer et al, 2014; Cui et al, 2015; Sun et al, 2015) and inhibition of autophagy in lung and kidney ischemic reperfusion injury (Lempiäinen et al, 2014; Xie et al, 2015). However, whether DEX regulates autophagy in cerebral ischemia-reperfusion injury is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine Protects Mouse Brain from Ischemia-Reperfusion Injury via Inhibiting Neuronal Autophagy through Up-Regulating HIF-1α

Luo

Ouyang

Fang

et al. 2017

Front. Cell. Neurosci.

100

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Stroke is the leading cause of death in China and produces a heavy socio-economic burden in the past decades. Previous studies have shown that dexmedetomidine (DEX) is neuroprotective after cerebral ischemia. However, the role of autophagy during DEX-mediated neuroprotection after cerebral ischemia is still unknown. In this study, we found that post-conditioning with DEX and DEX+3-methyladenine (3-MA) (autophagy inhibitor) reduced brain infarct size and improved neurological deficits compared with DEX+RAPA (autophagy inducer) 24 h after transient middle cerebral artery artery occlusion (tMCAO) model in mice. DEX inhibited the neuronal autophagy in the peri-ischemic brain, and increased viability and decreased apoptosis of primary cultured neurons in oxygen-glucose deprivation (OGD) model. DEX induced expression of Bcl-1 and p62, while reduced the expression of microtubule-associated protein 1 light chain 3 (LC3) and Beclin 1 in primary cultured neurons through inhibition of apoptosis and autophagy. Meanwhile, DEX promoted the expression of hypoxia-inducible factor-1α (HIF-1α) both in vivo and in vitro, and 2-Methoxyestradiol (2ME2), an inhibitor of HIF-1α, could reverse DEX-induced autophagic inhibition. In conclusion, our study suggests that post-conditioning with DEX at the beginning of reperfusion protects mouse brain from ischemia-reperfusion injury via inhibition of neuronal autophagy by upregulation of HIF-1α, which provides a potential therapeutic treatment for acute ischemic injury.

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“…It attenuates sympathetic tone, with reduction of the neuroendocrine and hemodynamic responses to anesthesia and surgery; decrease opioid and anesthetic requirements; and causes sedation without risk of respiratory depression. Many reports have noted other possible applications including use as a protective agent against ischemia/ reperfusion (I/R) injury in various organs [10,11], including heart [12], kidney [13], brain [14], lung [15], liver [16], and even retina [17]. Only three studies have addressed the roles of miRNAs in mechanisms of organ protection [14,18,19].…”

Section: Rongbi Liangmentioning

confidence: 99%

Circulating miRNA Expression Profiling and Target Prediction in Patients Receiving Dexmedetomidine

Yang

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Circulating miRNAs could serve as biomarkers for diagnosis or prognosis of heart diseases and cerebrovascular diseases. Dexmedetomidine has protective effects in various organs. The effects of dexmedetomidine on circulating miRNAs remain unknown. Here, we investigated differentially expressed miRNA and to predict the target genes of the miRNA in patients receiving dexmedetomidine. Methods: The expression levels of circulating miRNAs of 3 patients were determined through high through-put miRNA sequencing technology. Target genes of the identified differentially expressed miRNAs were predicted using TargetScan 7.1 and miRDB v.5. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to conduct functional annotation and pathway enrichment analysis of target genes respectively. Results: Twelve differentially expressed miRNAs were identified. Five miRNAs were upregulated (hsa-miR-4508, hsa-miR-novel-chr8_87373, hsa-miR-30a-3p, hsa-miR-novel-chr16_26099, hsa-miR-4306) and seven miRNAs (hsa-miR-744-5p, hsa-miR-320a, hsa-miR-novel-chr9_90035, hsa-miR-101-3p, hsa-miR-150-5p, hsa-miR-342-3p, and hsa-miR-140-3p) were downregulated after administration of dexmedetomidine in the subjects. The target genes and pathways related to the differentially expressed miRNAs were predicted and analyzed. Conclusion: The differentially expressed miRNAs may be involved in the mechanisms of action of dexmedetomidine. Specific miRNAs, such as hsa-miR-101-3p, hsa-miR-150-5p and hsa-miR-140-3p, are new potential targets for further functional studies of dexmedetomidine.

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The protective effects of dexmedetomidine against apoptosis in retinal ischemia/reperfusion injury in rats

Abstract: Dexmedetomidine is protective against apoptosis in retinal I/R injury in rats.

Cited by 17 publications

References 32 publications

The effect of swimming exercise on adenine-induced kidney disease in rats, and the influence of curcumin or lisinopril thereon

The effect of swimming exercise on adenine-induced kidney disease in rats, and the influence of curcumin or lisinopril thereon

Dexmedetomidine Protects Mouse Brain from Ischemia-Reperfusion Injury via Inhibiting Neuronal Autophagy through Up-Regulating HIF-1α

Circulating miRNA Expression Profiling and Target Prediction in Patients Receiving Dexmedetomidine

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