Ginsenosides are a class of active components extracted from ginseng plants (such as Panax ginseng, Panax quinquefolium, and Panax notoginseng). Ginsenosides have significant protective effects on the nervous system, cardiovascular system, and immune system, so they have been widely used in the treatment of related diseases. Entry of a variety of endogenous or exogenous harmful substances into the body can lead to an imbalance between the antioxidant defense system and reactive oxygen species, thus producing toxic effects on a variety of tissues and cells. In addition, oxidative stress can alter multiple signaling pathways, including the Keap1/Nrf2/ARE, PI3K/AKT, Wnt/β‐catenin, and NF‐κB pathways. With the deepening of research in this field, various ginsenoside monomers have been reported to exert antioxidant effects through multiple signaling pathways and thus have good application prospects. This article summarized the research advancements regarding the antioxidative effects and related mechanisms of ginsenosides, providing a theoretical basis for experimental research on and clinical treatment with ginsenosides.

Geraniin, a polyphenol isolated from Phyllanthus amarus, possesses extensive biological and pharmaceutical activities. In this study, we investigated the protective effect against cerebral ischemia/reperfusion (I/R) injury of geraniin and explored its potential mechanism. Middle cerebral artery occlusion/reperfusion (MCAO/R) was used to simulate cerebral I/R injury in vivo, and oxygen‐glucose deprivation/reoxygenation (OGD/R) was applied to establish an in vitro model of cerebral I/R injury. In this study, we performed TTC and HE staining and adopted a neurological score method to evaluate the neuroprotective effect of geraniin in vivo and used the CCK‐8 assay to assess this effect in vitro. Indices of reactive oxidation capacity were measured in vivo and in vitro to verify the antioxidant capacity of geraniin. TUNEL staining and flow cytometry were applied to measure the apoptosis rate, and Western blotting was performed to assess the expression of apoptosis‐related proteins. Finally, the expression of Nrf2 and HO‐1 was evaluated in vivo and in vitro by Western blotting. Geraniin significantly reduced the infarct volume, decreased neurological deficit scores, alleviated pathological changes in neurons, and increased the cell survival rate. Geraniin increased the activity of superoxide dismutase (SOD) and decreased the activity of lactate dehydrogenase (LDH) and the contents of malondialdehyde (MDA), nitric oxide (NO), and neuronal nitric oxide synthase (nNOS) in vivo and in vitro. In addition, geraniin significantly reduced the apoptosis. Furthermore, geraniin also evidently increased Nrf2 (total and nuclear) and HO‐1 protein expression in vivo and in vitro. Collectively, these results imply that geraniin may exert a protective effect against cerebral I/R injury by suppressing oxidative stress and neuronal apoptosis. The mechanism underlying the protective effect of geraniin is associated with activation of the Nrf2/HO‐1 pathway. Our results indicate that geraniin may be a potential drug candidate for the treatment of ischemic stroke.

Background: Panax notoginseng(Burk.) F. H. Chen (P. notoginseng) is a traditional Chinese medicine that has been used therapeutically for cardiovascular diseases, inflammatory diseases and traumatic injuries as well as for external and internal bleeding due to injury. Ginsenoside Rb1, a crucial monomeric active constituent extracted fromP. notoginseng, has attracted widespread attention because of its potential anti-inflammatory, bacteriostatic, and cell growth-promoting effects. In this study, the therapeutic effects of ginsenoside Rb1 on second-degree burn in rats and the potential underlying mechanisms were explored.Methods: A rat model of second-degree burn injury was established, and skin wound healing was monitored at different time points after ginsenoside Rb1 treatment. HE staining was performed to identify burn severity, and biological tissues were biopsied on days 0, 7, 14, and 24 after treatment. Skin wound healing at different time points was monitored by macroscopic observation. Furthermore, IHC, WB, and RT-PCR were utilized to determine the protein and mRNA expression levels of PDGF-BB, PDGFR-β, and FGF-2 in wound tissues after treatment.Results: HE staining showed that after 24 days of ginsenoside Rb1 treatment, skin tissue morphology was significant improved. Macroscopic observation demonstrated that in ginsenoside Rb1-treated rats, the scab removal time and fur growth time were decreased, and the wound healing rate was increased. Collectively, the results of IHC, WB and RT-PCR showed that PDGF-BB, PDGFR-β, and FGF-2 expressions peaked earlier in ginsenoside Rb1-treated rats than in model rats, consistent with the macroscopic observations.Conclusion: Collectively, these findings indicated that ginsenoside Rb1 promotes burn wound healing via a mechanism possibly associated with upregulation of FGF-2/PDGF-BB/PDGFR-β gene and protein expressions.