Research progress in pharmacological actions of ginsenoside-Rg3

Ginseng is a traditional Chinese medicine with a long medicinal history.Ginsenoside is the main compo⁃nent of ginseng,among which the ginsenoside-Rg3 possess higher medicinal value.The pharmacological studies reported that the ginsenoside-Rg3 exhibit a variety of pharmacological actions.For example,the ginsenoside-Rg3 exhibit an effective inhibitory effect against cancer and induce apoptosis,such as glioma,lung cancer,liver cancer,breast cancer,ovarian cancer,cervical cancer and so on.The anti-cancer effect will be significantly increased by combinning chemotherapy drugs with ginsenoside-Rg3.In addition,ginsenoside-Rg3 can reduce the side effects of chemotherapy drugs,such as cardiotoxicity and nephrotoxicity.Furthermore,ginsenoside-Rg3 could reverse the multidrug resistance of cancer cells against anticancer drugs.What′s more,ginsenoid-Rg3 has several other pharmacological actions as follows.At first,ginsenoid-Rg3 appears to anti-fatigue effect by reversing the dopamine reduction induced by fatigue.Secondly,ginsenoid-Rg3 can reverse chemical-induced memory damage and improve memory to exert neuroprotective effect.Finally,ginsenoid-Rg3 can improve mitochondrial function and insulin tolerance in skeletal muscle,suggesting that ginsenoid-Rg3 can be used as a hypoglycemic drug.In this review,I present an overview of the pharmacological actions of ginsenoside-Rg3 to provide theoretical guidance for further development and utilization of ginsenoside-Rg3.

Ginsenoside-Rg1 combined with a conditioned medium from induced neuron-like hUCMSCs alleviated the apoptosis in a cell model of ALS through regulating the NF-κB/Bcl-2 pathway

Amyotrophic lateral sclerosis(ALS)is a fatal neurodegenerative disease affecting both upper and lower motor neurons in the brain and spinal cord.One important aspect of ALS pathogenesis is superoxide dismutase 1(SOD1)mutant-mediated mitochondrial toxicity,leading to apoptosis in neurons.This study aimed to evaluate the neural protective synergistic effects of ginsenosides Rg1(G-Rg1)and conditioned medium(CM)on a mutational SOD1 cell model,and to explore the underlying mechanisms.We found that the contents of nerve growth factor,glial cell line-derived neurotrophic factor,and brain-derived neurotrophic factor significantly increased in CM after human umbilical cord mesenchymal stem cells(hUCMSCs)were exposed to neuron differentiation reagents for seven days.CM or G-Rg1 decreased the apoptotic rate of SOD1^(G93A)-NSC34 cell to a certain extent,but their combination brought about the least apoptosis,compared with CM or G-Rg1 alone.Further research showed that the anti-apoptotic protein Bcl-2 was upregulated in all the treatment groups.Proteins associated with mitochondrial apoptotic pathways,such as Bax,caspase 9(Cas-9),and cytochrome c(Cyt c),were downregulated.Furthermore,CM or G-Rg1 also inhibited the activation of the nuclear factor-kappa B(NF-κB)signaling pathway by reducing the phosphorylation of p65 and IκBa.CM/G-Rg1 or their combination also reduced the apoptotic rate induced by betulinic acid(BetA),an agonist of the NF-κB signaling pathway.In summary,the combination of CM and G-Rg1 effectively reduced the apoptosis of SOD1^(G93A)-NSC34 cells through suppresing the NF-κB/Bcl-2 sgaling pathway(Fig.1 is a graphcal representation of the abstract).