The effect of zinc acexamate on oxidative stress, inflammation and mitochondria induced apoptosis in rat model of renal warm ischemia

Abdallah, Najet Hadj; Baulies, Anna; Bouhlel, Ahlem; Béjaoui, Mohamed; Zaoualí, Mohamed Amine; Mimouna, Safa Ben; Messaoudi, Imed; Fernández-Checa, José C.; García-Ruiz, Carmen; Abdennebi, Hassen Ben

doi:10.1016/j.biopha.2018.06.017

Cited by 18 publications

(19 citation statements)

References 48 publications

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“…Zinc is an essential trace element with antioxidant [ 14 – 16 ] and anti-inflammatory [ 17 , 18 ] properties. It plays a critical role in neuronal signaling and is also known as a cofactor for antioxidant enzymes [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Zinc supplementation affects favorably the frequency of migraine attacks: a double-blind randomized placebo-controlled clinical trial

Ahmadi

Mazloumi-Kiapey

Sadeghi

et al. 2020

Nutr J

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Background Observational studies have shown a link between zinc deficiency and migraine headaches. We aimed to examine the effect of zinc supplementation on the characteristics of migraine attacks in patients with migraine. Methods This randomized clinical trial was conducted on 80 patients with migraine. Patients were randomly assigned to receive either zinc sulfate (220 mg/d zinc sulfate) or placebo (lactose) for 8 weeks. Anthropometric measures, serum zinc concentrations, and characteristics of migraine attacks (headache severity, frequency and duration of migraine attacks, and headache daily results) were assessed at baseline and end of the trial. Results Compared with the placebo, zinc supplementation resulted in a significant reduction in headache severity (− 1.75 ± 1.79 vs. -0.80 ± 1.57; P = 0.01) and migraine attacks frequency (− 2.55 ± 4.32 vs. -0.42 ± 4.24; P = 0.02) in migraine patients. However, the observed reduction for headache severity became statistically non-significant when the analysis was adjusted for potential confounders and baseline values of headache severity. Other characteristics of migraine attacks including the duration of attacks and headache daily results were not altered following zinc supplementation either before or after controlling for covariates. Conclusion Zinc supplementation had a beneficial effect on the frequency of migraine attacks in migraine patients. Additional well-designed clinical trials with a long period of intervention and different dosages of zinc are required. Trial registration code IRCT20121216011763N23 at www.irct.ir.

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Section: Introductionmentioning

confidence: 99%

Zinc supplementation affects favorably the frequency of migraine attacks: a double-blind randomized placebo-controlled clinical trial

Ahmadi

Mazloumi-Kiapey

Sadeghi

et al. 2020

Nutr J

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“…Zn as a protective agent against RIR was studied before, and it was shown that Zn improved RIR injury (14, 24, 25). Possibly, the antioxidant effect of Zn (26) is the major cause of this protection since Zn increases metallothionein production, which scavenges free radicals (OH) (27) and Zn deficiency disturbs lipid peroxidation system (28).…”

Section: Discussionmentioning

confidence: 99%

“…Zinc (Zn) is an essential element for the stability and activity of SOD, which its antioxidant effect was reported in RIR model (13, 14). Subcutaneous injection of Zn chloride also showed an intensive protective effect in reduction of tubular injury and necrosis.…”

Section: Introductionmentioning

confidence: 99%

Zinc Supplementation and Ischemia Pre-conditioning in Renal Ischemia/Reperfusion Injury

Mazaheri

Emami

Moslemi

et al. 2019

MJMS

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Backgrounds Renal ischemia/reperfusion (RIR) is a major cause of kidney dysfunction in clinic. The main objective of this study was to investigate the effect of pre-conditioning ischemia (IPC) and zinc (Zn) supplementation on renal RIR injury. Methods A total of 63 unilateral nephrectomised male and female Wistar rats were divided into five groups. Group 1 (ShOPR): Rats as sham-operated group were subjected to surgical procedure without RIR. Group 2 (Isch): Rats underwent RIR (left kidney ischemia for 30 min followed by 48 h reperfusion). Group 3 (Zn+Isch): Rats were treated as group 2 but they received Zn sulphate (30 mg/kg) 1 h before induction of RIR. Group 4 (IPC+Isch): Rats were treated as group 2 but they underwent 1 min of ischemia followed by 3 min reperfusion as IPC, which was repeated for three times before induction of RIR. Group 5 (Zn+IPC+Isch): Rats were subjected to receive both Zn sulphate and IPC before induction of RIR. Urine samples were collected in the last 6 h of reperfusion, and finally biochemical and histological measurements were performed. Results The serum level of creatinine (Cr), normalised kidney weight (KW) and kidney tissue damage score (KTDS) increased by RIR alone significantly ( P < 0.05). These parameters were attenuated statistically by Zn supplementation ( P < 0.05). However, IPC alone or co-treatment of Zn and IPC did not improve the biochemical and histological markers altered by RIR injury. Conclusion Zn supplementation had a protective role against RIR while such protective effect was not observed by IPC alone or by co-treatment of Zn and IPC.

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“…HO-1, heme oxygenase-1; Nrf2, nuclear factor erythroid 2-related factor 2; OGD/R, oxygen-glucose deprivation/reoxygenation; ROS, reactive oxygen species; si-Nrf2, small interfering RNA targeting Nrf2 proves that inhibition of oxidative stress may contribute to the attenuation of I/R injury. 16,17 In the present study, we used an OGD/R model to simulate cerebral I/R injury in primary hippocampal neurons. As expected, OGD/R stimulation caused cytotoxicity, oxidative stress, and apoptosis in hippocampal neurons.…”

Section: Discussionmentioning

confidence: 99%

Daphnetin protects hippocampal neurons from oxygen‐glucose deprivation–induced injury

Jin

Duan

Pei

et al. 2018

J of Cellular Biochemistry

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Daphnetin, a coumarin derivative extracted from Daphne odora var., was reported to possess a neuroprotective effect. Recently, it has been demonstrated that daphnetin attenuates ischemia/reperfusion (I/R) injury. However, the role of daphnetin in cerebral I/R injury and the potential mechanism have not been fully understood. The present study aimed to explore the regulatory roles of daphnetin on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced cell injury in a model of hippocampal neurons. Our results demonstrated that daphnetin improved cell viability and reduced the lactate dehydrogenase leakage in OGD/R-stimulated hippocampal neurons. In addition, daphnetin inhibited oxidative stress and cell apoptosis in hippocampal neurons after OGD/ R stimulation. Furthermore, daphnetin significantly enhanced the nuclear translocation of the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression in hippocampal neurons exposed to OGD/R. Knockdown of Nrf2 blocked the protective effect of daphnetin on OGD/ R-induced hippocampal neurons. In conclusion, these findings demonstrated that daphnetin attenuated oxidative stress and neuronal apoptosis after OGD/R injury through the activation of the Nrf2/HO-1 signaling pathway in hippocampal neurons. Thus, daphnetin may be a novel therapeutic agent for cerebral I/R injury. K E Y W O R D S cerebral ischemia/reperfusion (I/R) injury, daphnetin, hippocampal neurons, neuroprotective, Nrf2/HO-1 pathway, oxidative stress How to cite this article: Zhi J, Duan B, Pei J, Wu S, Wei J. Daphnetin protects hippocampal neurons from oxygen-glucose deprivation-induced injury.

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The effect of zinc acexamate on oxidative stress, inflammation and mitochondria induced apoptosis in rat model of renal warm ischemia

Cited by 18 publications

References 48 publications

Zinc supplementation affects favorably the frequency of migraine attacks: a double-blind randomized placebo-controlled clinical trial

Zinc supplementation affects favorably the frequency of migraine attacks: a double-blind randomized placebo-controlled clinical trial

Zinc Supplementation and Ischemia Pre-conditioning in Renal Ischemia/Reperfusion Injury

Daphnetin protects hippocampal neurons from oxygen‐glucose deprivation–induced injury

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