Curcumin Protects Human Umbilical Vein Endothelial Cells against H₂O₂-Induced Cell Injury

Abstract

Migraine is a prevalent neurological disorder which causes a huge economic burden on society. It is thought to be a neurovascular disease with oxidative stress might be involved. Curcumin, one of the major ingredients of turmeric, has potent antioxidative and anti-inflammatory properties, but whether it could be used as a potential treatment for migraine remains to be explored. In the present study, human umbilical vein endothelial cells (HUVECs) were pretreated with various concentrations of curcumin (0 μM, 10 μM, 20 μM, 30 μM, 40 μM, and 50 μM) for 12 h, thereby exposed to H2O2 (100 μM) for another 12 h. The viability of HUVECs was tested by the CCK-8 assay, and the activities of antioxidant enzymes including superoxide dismutase (SOD) and glutathione (GSH) were also examined. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were assayed to determine H2O2-induced oxidative stress. In addition, several cell death-related genes (p53, p21, Bax, and Bcl-2) were detected by PCR, and an apoptosis-related protein (caspase3) was evaluated by western blotting. Our results showed that curcumin improved the H2O2-induced decrease of cell viability and antioxidative enzyme activities and decreased the level of oxidative stress. As a conclusion, curcumin could mitigate H2O2-induced oxidative stress and cell death in HUVECs and may be a potential therapeutic drug for migraine.

Protective effects ofNigella sativaextract against H2O2‐induced cell death through the inhibition of DNA damage and cell cycle arrest in human umbilical vein endothelial cells (HUVECs)

“…The functional damage of vascular endothelial cells is elaborated in the formation of the acute myocardial ischemia and atherosclerosis (Gimbrone & García‐Cardeña, 2016). HUVECs are the most frequent used in vitro model system for assessing the mechanisms involved in the of cytotoxicity and cyto‐protection to endothelium (Shen et al, 2013; Yang et al, 2015; Safaeian, Javanmard, Mollanoori, & Dana, 2015; Babaee, Safaeian, Zolfaghari, & Javanmard, 2016; Cao et al, 2017; Ouyang, Li, Shi, & Zhong, 2019). In the present investigation, we have chosen HUVECs as an in vitro model system to study the probable protective potential of NSE against H 2 O 2 ‐induced cellular damages.…”

“…Hydrogen peroxide (H 2 O 2 ) belongs to ROS, readily crosses cell membrane, and generates extremely reactive free radicals that can damage cells and tissues (Bienert, Schjoerring, & Jahn, 2006). H 2 O 2 has extensively been used to induce cytotoxicity and oxidative stress in human umbilical vein endothelial cells (HUVECs) as an in vitro model (Shen et al, 2013; Yang et al, 2015; Safaeian, Javanmard, Mollanoori, & Dana, 2015; Babaee, Safaeian, Zolfaghari, & Javanmard, 2016; Tian et al, 2017; Ouyang, Li, Shi, & Zhong, 2019). Since H 2 O 2 has the ability to induce HUVECs dysfunction and apoptosis (Song, Pu, & He, 2014), therefore, H 2 O 2 was considered as an inducer of HUVECs cell death.…”

An investigation of oxidant/antioxidant balance in patients with migraine: a case-control study

“…Based on the relevant literature of animal and human studies, the elevated level of this oxidative mediator has been linked to cortical spreading depression (CSD), one of the main proposed pathological mechanisms in migraine pain initiation particularly in migraine with aura [10, 22, 23, 25, 27, 33–35]. As such, it has been suggested that MDA levels may be attenuated following administration of curcumin, a dietary agent with antioxidant features, in umbilical vein endothelial cells which were considered a model for exploring oxidative stress status in migraine [36].…”

Zearalenone Induces Endothelial Cell Apoptosis through Activation of a Cytosolic Ca2+/ERK1/2/p53/Caspase 3 Signaling Pathway

“…Once drugs and/or chemicals are ingested, they first contact the EC lining of the blood vessels and other cellular matrices before reaching their target sites. Studies have shown that ECs can be easily damaged by various stressors, such as cigarette aerosol, H 2 O 2 , and oxygen-glucose deprivation/reperfusion [ 15 , 16 , 17 ]. These factors can cause DNA damage and inflammation, which eventually lead to death of ECs, and weaken the integrity and function of blood vessels.…”