Ginsenoside Rg2 Attenuates Aging-Induced Liver Injury via Inhibiting Caspase 8-Mediated Pyroptosis, Apoptosis and Modulating Gut Microbiota.

Aging is an irresistible natural law of the progressive decline of body molecules, organs, and overall function with the passage of time, resulting in eventual death. World Health Organization data show that aging is correlated with a wide range of common chronic diseases in the elderly, and is an essential driver of many diseases. Panax Ginseng C.A Meyer is an ancient herbal medicine, which has an effect of "long service, light weight, and longevity" recorded in the ancient Chinese medicine book "Compendium of Materia Medica." Ginsenoside Rg2, the main active ingredient of ginseng, also exerts a marked effect on the treatment of liver injury. However, it remains unclear whether Rg2 has the potential to ameliorate aging-induced liver injury. Hence, exploring the hepatoprotective properties of Rg2 and its possible molecular mechanism by Senescence Accelerate Mouse Prone 8 (SAMP8) and gut microbiota. Our study demonstrated that Rg2 can inhibit pyroptosis and apoptosis through caspase 8, and regulate the gut-liver axis to alleviate liver inflammation by changing the composition of gut microbiota, thus improving aging-induced liver injury. These findings provide theoretical support for the pharmacological effects of ginsenosides in delaying aging-induced liver injury.

Ginsenoside Rg5: A Review of Anticancer and Neuroprotection with Network Pharmacology Approach.

Ginsenoside Rg5 (G-Rg5) is a rare ginsenoside isolated from ginseng (Panax ginseng C.A. Meyer), and this compound is increasingly known for its potent pharmacological activities. This study aimed to provide a comprehensive review of the main activities and mechanisms of G-Rg5 by adopting network pharmacological analysis combined with a summary of published articles. The 100 target genes of G-Rg5 were searched through available database, subjected to protein-protein interaction (PPI) network generation and then core screening. The results showed that G-Rg5 has promising anticancer and neuroprotective effects. By summarizing these two pharmacological activities, we found that G-Rg5 exerts its therapeutic effects mainly through PI3K/AKT, MAPK signaling pathways, and the regulation of apoptosis and cell cycle. And these results were corroborated by KEGG analysis. Likewise, molecular docking of the related proteins was performed, and the binding energies were all less than [Formula: see text]7.0[Formula: see text]kJ/mol, indicating that these proteins had excellent binding capacity with G-Rg5. The network pharmacology results revealed many potential G-Rg5 mechanisms, which need to be further explored. We expect that the network pharmacology approach and molecular docking techniques can help us gain a deeper understanding of the therapeutic mechanisms of different ginsenosides and even the ginseng plant, for further developing their therapeutic potential as well as clinical applications.

Arabinogalactan derived from Larix gmelinii (Rupr.) Kuzen. Alleviates cisplatin-induced acute intestinal injury in vitro and in vivo through IRE1α/JNK axis mediated apoptotic signaling pathways.

Many dietary polysaccharides have been shown to protect against various harmful external stimuli by protecting the integrity of the intestinal barrier. Arabinogalactan (AG) is a high molecular weight polysaccharide composed of arabinose and galactose, which has good immunomodulatory, antioxidant and intestinal conditioning activities. Gastrointestinal injury caused by cisplatin (CP) is an inevitable damage during CP chemotherapy. This research explored the ameliorative effect of AG on cisplatin-induced intestinal toxicity and its possible molecular targets and mechanisms. The results showed that AG (200, 400 mg/kg) could significantly reverse the intestinal histopathological changes and oxidative stress injury caused by CP. Meantime, AG could target the IRE1α/JNK axis to inhibit the expression of apoptosis-related proteins and block the apoptotic cascade, thus reducing intestinal damage. In vitro, AG (10, 20, and 40 µg/mL) could regulate the IRE1α/JNK axis, inhibit apoptosis, and restore the antioxidant defense system damaged by CP to play a protective role in the intestine. In addition, 4-phenylbutyrate (4-PBA), a specific inhibitor of endoplasmic reticulum stress, was used to verify that AG also affected protein expression levels by regulating the IRE1α/JNK pathway-mediated endoplasmic reticulum stress signaling pathway, thereby alleviating CP-induced gastrointestinal dysfunction. Therefore, AG may be a potential drug to prevent CP-induced intestinal damage.