Preincubation with a low-dose hydrogen peroxide enhances anti-oxidative stress ability of BMSCs

Abstract

Objective To investigate the effects of low-concentration hydrogen peroxide pretreatment on the anti-oxidative stress of the bone marrow mesenchymal stem cells (BMSCs). Methods Rabbit BMSCs were isolated and cultured by density gradient centrifugation combined with the adherence method. Then, the third generation of well-grown BMSCs was continuously treated with 50-μM hydrogen peroxide (H2O2) for 8 h as the optimal pretreatment concentration and the BMSCs were continuously applied for 24 h with 500 μM H2O2, and the optimal damage concentration was determined as the oxidative stress cell model. The experiment was divided into three groups: control group, high-concentration H2O2 injury group (500 μM), and low-concentration H2O2 pretreatment group (50 μM + 500 μM). In each group, the DCFH-DA fluorescence probe was used to detect the reactive oxygen species (ROS). ELISA was used to detect the activity of superoxide dismutase (SOD) and catalase (CAT), and the TBA method was used to detect malondialdehyde (MDA). The mitochondrial membrane potential was detected by JC-1. The cell viability was detected by CCK-8 method, while flow cytometry and TUNEL/DAPI double staining were performed to detect cell apoptosis. Hence, the effect of H2O2 pretreatment on the anti-oxidative stress of BMSCs was investigated. One-way analysis of variance was performed using SPSS 19.0 statistical software, and P < 0.05 was considered statistically significant. Results A large number of typical BMSCs were obtained by density gradient centrifugation and adherent culture. The oxidative stress cell model was successfully established by 500-μM H2O2. Compared with the high-concentration H2O2 injury group, the low-concentration H2O2 pretreatment reduced the production of ROS [(62.33 ± 5.05), P < 0.05], SOD and CAT activities significantly increased (P < 0.05), and MDA levels significantly decreased (P < 0.05). The mitochondrial membrane potential fluorescence changes, the ratio of red/green fluorescence intensity of the high-concentration H2O2 injury group was less, and the ratio of the low-concentration H2O2 pretreatment group was significantly higher than that. The ratio of red/green increased by about 1.8 times (P < 0.05). The cell viability and survival rate of BMSCs were significantly increased in low-concentration H2O2 pretreatment group (P < 0.05), and the cell apoptosis rate was significantly decreased (P < 0.05). Conclusion Pretreatment with low-concentration H2O2 can enhance the anti-oxidative stress ability and reduce their apoptosis of BMSCs under oxidative stress.

Ultrasonic treatment decreases Lyophyllum decastes fruiting body browning and affects energy metabolism

“…Antioxidant enzymes reduce tissue oxidative damage, delay fruit and vegetable senescence after harvest and maintain high commodity acceptance [7] . CAT and POD activities reduce intracellular reactive oxygen species and cell apoptosis [39] , [40] . In this work, mushrooms treated with US maintained higher CAT and POD activities compared with the CK sample ( Fig.…”

Effect of Oxidative Stress-Induced Autophagy on Proliferation and Apoptosis of hMSCs

“…Excessive autophagy will induce cell apoptosis. The occurrence of cell apoptosis is a complex process involving many factors, such as ROS production, mitochondrial depolarization, chromatin agglutination and nuclear division [4]. After H2O2 interferes with hBMSCs, it activates the oxidative stress response and reduces the level of cell apoptosis, which proves that low-concentration H2O2 pretreatment can signi cantly increase the cell survival rate of hBMSCs after oxidative stress damage and inhibit cell apoptosis.…”

“…However, when harmful stimuli occur, a large amount of reactive oxygen species will be produced, and the antioxidant system's ability to remove these reactive oxygen species is limited, eventually leading to oxidative damage [11]. Excessive ROS will increase mitochondrial membrane permeability, mitochondrial swelling, mitochondrial permeability (mMPTP) opening and mitochondrial DNA (mtDNA) damage [4]. This experiment shows that low-concentration H2O2 pretreatment activates the oxidative stress response, which can signi cantly increase the resistance of hBMSCs to oxidative stress, reduce the production of intracellular ROS, and reduce cell oxidative stress damage.…”

“…Oxidative stress is the key cause of the death of transplanted bone marrow mesenchymal stem cells [3]. The important mechanism is that the oxidative stress microenvironment of the osteonecrosis area increases the production of ROS and/or reduces the ability to remove ROS, which leads to an imbalance between ROS production and removal [4].…”

Mesenchymal stem cell-derived exosomes for gastrointestinal cancer

“…Despite that both MSCs and MSC-derived exosomes can be used in anti-cancer research, MSC-derived exosomes show many potential advantages. First, MSC transplantation may result in the transfer of mutated or damaged DNA into normal cells, and an increasing risk of a new disease[ 136 ]. Fortunately, if MSC-derived exosomes are directly transferred into the body, these problems can be effectively avoided.…”