Neuroprotective Effects of Hesperidin on Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage in Rats: Biochemical, Pathologic, and Histomorphometric Analysis

Aydoğmuş, Evren; Gül, Şanser; Bahadir, Burak

doi:10.1016/j.wneu.2018.11.043

Cited by 6 publications

(14 citation statements)

References 28 publications

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“…Blood in the subarachnoid space has an irritant effect, which leads to vasospasm by activating antiinflammatory mechanisms [7]. Early brain injury, seizures, CV, and delayed cerebral ischaemia are important factors contributing to the poor prognosis of SAH [1]. As CV is the leading cause of morbidity and mortality, there have been many experimental animal studies to develop effective treatments [6,7].…”

Section: Discussionmentioning

confidence: 99%

“…However, there is still only limited information about the underlying mechanism of CV. Current treatments for CV following SAH include triple-H therapy (hypertension, hypervolemia, haemodilution), prophylactic hyperdynamic postoperative fluid therapy, and drug therapy [1,6]. As these SAH treatments have not been definitely proven to prevent CV, a number of experimental treatment strategies have been proposed, such as antioxidant drug therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Although there are many different mechanisms of free radical production after SAH, autooxidation of haemoglobin is thought to be the main source as soon as it is released into the subarachnoid space [9]. SAH induces the enzymes responsible for reactive oxygen species (ROS) and inhibits the intracellular antioxidant systems [1].…”

Section: Discussionmentioning

confidence: 99%

“…Cerebral vasospasm (CV) is the most important cause of morbidity and mortality following subarachnoid haemorrhage (SAH) [1]. The aim of SAH treatment is to prevent secondary brain injury by optimising cerebral blood blow, reducing cerebral metabolic demand, and avoiding hypoxia [2].…”

Section: Introductionmentioning

confidence: 99%

“…The experimental model was constructed as described previously [1,3,5]. Rats were anaesthetised by intraperitoneal injection of ketamine (60 mg/kg) and xylazine (10 mg/kg).…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effects of quercetin on cerebral vasospasm following experimental subarachnoid haemorrhage in rats

Gül¹,

Aydoğmuş²,

Bahadir³

et al. 2020

Turk J Med Sci

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The experimental protocol was approved by the Ethics Committee of Zonguldak Bülent Ecevit University. The study was conducted on thirty-eight male albino Wistar Background/aim: We examined the protective effects of the natural flavonoid, quercetin, against cerebral vasospasm in an experimental rat subarachnoid haemorrhage (SAH) model. Materials and methods: Thirty-eight albino Wistar rats were divided into five groups as follows: group 1 (G1, n=8), no experimental intervention; group 2 (G2, n=8), subarachnoid physiological saline; group 3 (G3, n=8), SAH; group 4 (G4, n=7) SAH and low-dose (10 mg/kg) quercetin treatment; group 5 (G5, n=7), SAH and high-dose (50 mg/kg) quercetin treatment. Subarachnoid haemorrhage was induced by injection of 0.15 cc of autologous blood taken from the tail artery into the cisterna magna from the craniocervical junction and basilar arteries and blood samples were taken for biochemical and histopathological analyses. Results: Malondialdehyde (MDA) levels were significantly higher in G2 and G3 than in G1 (P < 0.05). Significant decreases in MDA were observed in G4 and G5 compared with G2 (P < 0.05, G4-G2; P < 0.05, G5-G2). There were no significant differences between G2 and G3 or among G1, G4, and G5. No statistically significant differences were found in total antioxidant capacity between the groups (P > 0.05). There were no significant differences in basilar artery (BA) wall thickness between G3 and G4 or between G3 and G5, but G4 and G5 showed greater luminal diameters than G3 (P < 0.05). There were no significant differences in BA thickness or luminal diameter between G4 and G5. Conclusion: Our results suggested that quercetin may be beneficial in SAH therapy by preventing vasospasm.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…The experimental model was constructed as described previously [1,3,5]. Rats were anaesthetised by intraperitoneal injection of ketamine (60 mg/kg) and xylazine (10 mg/kg).…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effects of quercetin on cerebral vasospasm following experimental subarachnoid haemorrhage in rats

Gül¹,

Aydoğmuş²,

Bahadir³

et al. 2020

Turk J Med Sci

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Hesperidin protects against the chlorpyrifos‐induced chronic hepato‐renal toxicity in rats associated with oxidative stress, inflammation, apoptosis, autophagy, and up‐regulation of PARP‐1/VEGF

Küçükler

Çomaklı

Özdemir

et al. 2021

Environmental Toxicology

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In this study, we investigated the effects of hesperidin (HSP) on oxidants/antioxidants status, inflammation, apoptotic, and autophagic activity in hepato-renal toxicity induced by chronic chlorpyrifos (CPF) exposure in rats. We used a total of 35 male albino rats in five groups of seven: control, HSP 100, CPF, CPF + HSP50, and CPF + HSP100. After rats were sacrificed, blood, liver, and kidney samples were collected.Serum levels of aspartate aminotransferases (ALT and AST), alkaline phosphatase (ALP), creatinine, and urea were tested. Then, contents of the superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GPx), and glutathione (GSH) were measured to detect the level of oxidative stress in rat liver and renal tissues. We measured inflammatory and autophagy markers of chlorpyrifos induced oxidative stress in the liver and kidney tissues including TNF-α, iNOS, IL-1 β, COX-2, NF-κB, MAPK14, and Beclin-1 using ELISA. Histopathological findings were also examined followed by immunohistochemical determination of 8-OHdG expression. Real-time PCR (RT-PCR) was used to examine Cas-3, Bax, Bcl-2, PARP-1, and VEGF, which are associated with apoptosis, autophagy, DNA, and endothelial damage, respectively. In addition, PARP-1 activity was supported by western blot and immunofluorescence, VEGF activity was supported by western blot methods. Treatment with HSP reduced the effect of CPF on ALT, AST, ALP, and total proteins, and increased its effect on tissue antioxidants. PARP/VEGF, apoptotic, pro-apoptotic, anti-apoptotic, and autophagic gene expressions were regulated, and Caspase-3 and Bax expressions were decreased; Bcl-2 expression increased in both the liver and kidney samples, and positivity of 8-OHdG and PARP-1 were reduced in the CPF plus

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Cerebroprotective Potential of Hesperidin Nanoparticles Against Bilateral Common Carotid Artery Occlusion Reperfusion Injury in Rats and In silico Approaches

Kumar¹,

Kumar

Nainita³

et al. 2019

Neurotox Res

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Neuroprotective Effects of Hesperidin on Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage in Rats: Biochemical, Pathologic, and Histomorphometric Analysis

Cited by 6 publications

References 28 publications

Neuroprotective effects of quercetin on cerebral vasospasm following experimental subarachnoid haemorrhage in rats

Neuroprotective effects of quercetin on cerebral vasospasm following experimental subarachnoid haemorrhage in rats

Hesperidin protects against the chlorpyrifos‐induced chronic hepato‐renal toxicity in rats associated with oxidative stress, inflammation, apoptosis, autophagy, and up‐regulation of PARP‐1/VEGF

Cerebroprotective Potential of Hesperidin Nanoparticles Against Bilateral Common Carotid Artery Occlusion Reperfusion Injury in Rats and In silico Approaches

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