Abstract
AimsIn this study, the efficacy of proanthocyanidins (PCs) against oxidative damage was systematically reviewed to facilitate their use in various applications.MethodsA meta-analysis was performed by two researchers. Each investigator independently searched electronic databases, including Cochrane, PubMed, Springer, Web of Science, China National Knowledge Infrastructure (CKNI), China Science and Technology Journal Database (CSTJ), and WanFang Data, and analyzed published data from 29 studies on the effects of PCs against oxidative damage. Oxidative stress indexes included superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), and total antioxidative capacity (T-AOC).ResultsCompared with the oxidative damage model group, PCs effectively improved the T-AOC, SOD, GSH, GPx, and CAT levels, and reduced the MDA levels; these differences were statistically significant (P < 0.05). In studies that used the gavage method, SOD (95% CI, 2.33–4.00) and GPx (95% CI, 2.10–4.05) were 3.16-fold and 3.08-fold higher in the PC group than in the control group, respectively. In studies that used the feeding method, SOD (95% CI, 0.32–1.74) and GPx (95% CI, -0.31 to 1.65) were 1.03-fold and 0.67-fold higher in the PC group than in the control group, respectively. Statistically significant differences in the effects of PCs (P < 0.00001) were observed between these two methods. MDA estimated from tissue samples (95% CI, -5.82 to -2.60) was 4.32-fold lower in the PC group than in the control group. In contrast, MDA estimated using serum samples (95% CI, -4.07 to -2.06) was 3.06-fold lower in the PC group than in the control group. The effect of PCs on MDA was significantly greater in tissue samples than in serum samples (P = 0.02).ConclusionPCs effectively antagonize oxidative damage and enhance antioxidant capacity. The antagonistic effect may be related to intervention time, intervention method, and the source from which the indexes are estimated.
Highlights
Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the ability of a biological system to eliminate ROS or repair the resulting damage [1]
In studies that used the gavage method, superoxide dismutase (SOD) and glutathione peroxidase (GPx) were 3.16-fold and 3.08-fold higher in the PC group than in the control group, respectively
In studies that used the feeding method, SOD and GPx were 1.03-fold and 0.67-fold higher in the PC group than in the control group, respectively
Summary
Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the ability of a biological system to eliminate ROS or repair the resulting damage [1]. Oxidative stress may result in an increased number of free radicals and cause lipid peroxidation, eventually leading to apoptosis and many diseases [2]. Increasing evidence has shown that oxidative stress plays a important role in the development of cardiovascular diseases such as atherosclerosis, hypertension, atrial fibrillation, and cardiomyopathy [3]. Many reactive substances, such as arsenic [4] and hydrogen peroxide (H2O2) [5], can result in organismal damage via ROS and oxidative stress. PCs have high antioxidant capacities and are efficient free radical scavengers.
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