Neuroprotective effect of p-coumaric acid in mice with cerebral ischemia reperfusion injuries

Abstract

Cerebral ischemia reperfusion (IR) is associated with neuronal death, which leads to disability and cognitive decline. The pathomechanism occurs because ischemia is exacerbated during the reperfusion period. Neuronal damage susceptibility depends on the affected brain areas and the duration of ischemia. Prevention and supplementation to neurons may help them endure during IR and further benefit them in rehabilitation. We investigated the protective effect of p-coumaric acid (PC) on cerebral IR injuries in mice. We randomly divided 30 male ICR mice into 3 groups of Sham (received vehicle and not induced IR), Control-IR (received vehicle and induced IR) and PC-IR (received 100 mg/kg PC and induced IR). We orally administered vehicle or 100 mg/kg of p-coumaric acid for 2 weeks before inducing the cerebral IR injuries by using 30 min of a bilateral common carotid artery occlusion followed by a 45-min reperfusion. We induced the IR condition in the Control-IR and PC-IR groups but not the Sham group, and only the PC-IR group received p-coumaric acid. After IR induction, we sacrificed all the mice and collected their brain tissues to evaluate their oxidative statuses, whole brain infarctions and vulnerable neuronal deaths. We studied the whole-brain infarction volume by 2, 3, 5-triethyltetrazoliumchloride staining of sections. We performed a histological investigation of the vulnerable neuronal population in the dorsal hippocampus by staining brain sections with 0.1% cresyl violet. The results indicated that IR caused significant increases in calcium and malondialdehyde (MDA) levels, whole brain infarction volume and hippocampal neuronal death. Pretreatment with p-coumaric acid significantly reduced MDA levels, whole-brain infarction volume and hippocampal neuronal death together and increased catalase and superoxide dismutase activities. We conclude here that pretreating animals with p-coumaric acid can prevent IR-induced brain oxidative stress, infarction size and neuronal vulnerability to death in cerebral IR injuries.

Neuroprotective Effect of Danhong Injection on Cerebral Ischemia-Reperfusion Injury in Rats by Activation of the PI3K-Akt Pathway

“…Fan et al found that salvianolic acid B has neuroprotective effect on brain injury induced by ischemia-reperfusion injury in rats by reducing the generation of free radicals, and which may be an effective clinical candidate treatment (Fan et al, 2018). During the research, Sakamula et al found that pretreatment with p-coumaric acid can significantly reduce malondialdehyde levels, whole cerebral infarct volume, and hippocampal neuron death, and increase catalase and superoxide dismutase activities, eventually producing neuroprotective effect (Sakamula and Thong-asa, 2018).…”

The Effects of P-Hydroxycinnamic Acid in Ameliorating Spatial Learning and Flexibility Deficits in Rats with Chronic Cerebral Hypoperfusion

“…Therefore, the present study cannot claim the effects of pHCA against brain oxidative stress. However, some evidence implied pHCA's benefits against oxidative stress in severely ischemic conditions (Guven et al 2015;Sakamula & Thong-Asa 2018).…”

“…The biochemical parameters for assessing brain oxidative status, such as total protein, malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) activities, were obtained by using the colorimetric method as previously described (Sakamula & Thong-Asa 2018).…”

“…It exerts a beneficial effect in free oxygen radical scavengers (Tanyeli 2018); improves mitochondrial function by decreasing apoptotic proteins; and increases nuclear respiratory factor (NRF-1), anxiolytic, anti-diabetic, anti-inflammatory, anti-cancer and anti-platelet aggregation (Abdel-Wahab 2003;Amalan 2016;Guven et al 2015). Recently, a neuroprotective effect against ischemic-reperfusion injury has been found (Sakamula & Thong-Asa 2018). Currently, the effects of pHCA on cognitive abilities associated with neurodegeneration have not been studied; therefore, the present study's aim is to investigate the effects of pHCA against cognitive impairments in rats with CCH induced by 2VO in relation to vulnerable neurodegeneration.…”

Effect of Tiliacora triandra Leaf Extract on Glycemic Control in Mice with High Sugar Intake

“…The organ tissues of the brain, liver, heart, lung, stomach, kidney, and testes were collected for biochemical analysis of the total protein (Lowry et al 1951), calcium (Spare 1964), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) and for indexing the organ oxidative status (Sakamula & Thong-Asa 2018).…”