The aim of the present study was to examine the neuroprotective effects of a panel of active components of ginseng and to explore their molecular mechanisms of action in two rotenone (Rot)‑induced models of Parkinson's disease: An in vitro model using the human neuroblastoma cell line SH‑SY5Y and an in vivo model using Drosophila. Ginsenoside Re (Re) was identified as the most potent inhibitor of Rot‑induced cytotoxicity in SH‑SY5Y cells by Cell Counting kit‑8 assay and lactate dehydrogenase release assay. Flow cytometry, Hoechst staining, Rhodamine 123 staining, ATP and cytochrome c release revealed that Re rescue of Rot‑induced mitochondrial dysfunction and inhibition of the mitochondrial apoptotic pathway. Western blot analysis demonstrated that Re alleviated Rot‑induced oxidative stress by activating the nuclear factor erythroid 2‑related factor 2 (Nrf2) anti‑oxidant pathway, and these effects were abolished by RNA interference‑mediated knockdown of Nrf2. Re enhanced phosphorylation of components of the phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (AKT) and extracellular regulated protein kinase (ERK) pathways, and pharmacological inhibition of these pathways reduced Re‑mediated Nrf2 activation and neuroprotection. In the Drosophila model, Immunofluorescence microscopy, reactive oxygen species (ROS), hydrogen peroxide and knockdown analysis revealed that Re reversed Rot‑induced motor deficits and dopaminergic neuron loss while concomitantly alleviating Rot‑induced oxidative damage. The findings of the present study suggest that Re protects neurons against Rot‑induced mitochondrial dysfunction and oxidative damage, at least in part, by inducing Nrf2/heme oxygenase‑1 expression and activation of the dual PI3K/AKT and ERK pathways.

To examine the protective effect and mechanism of the original extract of Dendrobium officinale (DE) on gastric lesions caused by aspirin (ASA) facilitate the development of traditional Chinese medicine products. In this study, a gastric lesions rat model was established, and then the rats were treated with DE for 5 days. We found that ASA-induced gastric mucosal detachment and hemorrhagic lesions in rats improved after DE supplementation. Meanwhile, effectively inhibits the secretion of inflammatory mediators (IL-6, IL-1β, TNF-α, MPO, COX-2) and upregulates the activity of antioxidant core components (T-SOD, GSH-Px) and defense factors (TFFs, EGF, EGFR) in gastric tissues. It was further found that DE exerted a defensive effect on the gastric mucosa in association with NF-κB/Nrf-2/HO-1 signaling. In conclusion, DE protects the gastric mucosa from oxidative stress, improves its defenses, as well as being a potential gastric mucosal nutrient in the future, preventing ASA-induced gastric lesions.

Ginsenosides, active substances in Panax ginseng C. A. Meyer (ginseng), extend lifespan in multiple species, ameliorate age-associated damage, and limit functional decline in multiple tissues. However, their active components and their molecular mechanisms are largely unknown. Here, ginsenoside Rg1 (Rg1) promoted longevity in Saccharomyces cerevisiae. Treatment with Rg1 decreased aging-mediated surface wrinkling, enhanced stress resistance, decreased reactive oxygen species’ production and apoptosis, improved antioxidant enzyme activity, and decreased the aging rate. Proteomic analysis indicated that Rg1 delays S. cerevisiae senescence by regulating metabolic homeostasis. Protein–protein interaction networks based on differential protein expression indicated that CDC19, a homologue of pyruvate kinase, and SDH2, the succinate dehydrogenase iron–sulfur protein subunit, might be the effector proteins involved in the regulation by Rg1. Further experiments confirmed that Rg1 improved specific parameters of mitochondrial bioenergetics and core enzymes in the glycolytic pathway. Mutant strains were constructed that demonstrated the relationships between metabolic homeostasis and the predicted target proteins of Rg1. Rg1 could be used in new treatments for slowing the aging process. Our results also provide a useful dataset for further investigations of the mechanisms of ginseng in aging.