Red ginseng and cancer treatment

The ginseng family,including Panax ginseng(Asian ginseng),Panax quinquefolius(American ginseng),and Panax notoginseng(notoginseng),is commonly used herbal medicine.White ginseng is prepared by air-drying after harvest,while red ginseng is prepared by a steaming or heating process.The anticancer activity of red ginseng is significantly increased,due to the production of active anticancer ginsenosides during the steaming treatment,compared with that of white ginseng.Thus far,anticancer studies have been mostly focused on Asian ginseng.In this article,we review the research progress made in the anticancer activities of red Asian ginseng,red American ginseng and red notoginseng.The major anticancer mechanisms of red ginseng compounds include cell cycle arrest,induction of apoptosis/paraptosis,and inhibition of angiogenesis.The structure-function relationship analysis has revealed that the protopanaxadiol group ginsenosides have more potent effects than the protopanaxatriol group.Sugar molecules in ginsenosides inversely impact the antiproliferative potential of these compounds.In addition,ginsenoside stereoselectivity and double bond position also influence the anticancer activity.Future studies should focus on characterizing active red ginseng derivatives as potential anticancer drugs.

Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson's Disease

Objective： To investigate the neuro-protective effects of Acanthopanax senticosus Harms（EAS） on mesencephalic mitochondria and the mechanism of action, using a mouse model of Parkinson＇s disease（PD）. Methods： The chemical fingerprint analysis of the extract of Acanthopanax senticosus Harms（EAS） was performed using the ultra performance liquid chromatograph and time of flight mass spectrometry. Thirty mice were randomly divided into the control group, the MPTP model group, and the EAS treated group with MPTP（MPTP＋EAS group, 10 in each group）. The MPTP model group and the MPTP＋EAS group received MPTP-HCl（30 mg/kg i.p） once a day for 5 days. The control group received an equal volume of saline（20 m L/kg i.p） once a day for 5 days. Induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine hydrochloride daily（MPTP-HCl, 30 mg/kg） for 5 days, the PD mice were treated with EAS at 45.5 mg/kg daily for 20 days. The behavioral testing of mice was carried out using the pole-climbing test. The integrity and functions of neurons were examined in mesencephalic mitochondria in a PD mouse model, including nicotinamide adenine dinucleotide dehydrogenase ubiquinone flavoprotein 2（NDUFV2）, mitochondrially encoded nicotinamide adenine dinucleotide dehydrogenase 1（MT-ND1）, succinate dehydrogenase complex subunit A（SDHA）, and succinate dehydrogenase cytochrome b560 subunit（SDHC）. Results： After treatment with EAS, the behavioral changes induced by MPTP were attenuated significantly（P〈0.05）. EAS protected the mesencephalic mitochondria from swelling and attenuated the decreases in their membrane potential（both P〈0.05）, which was supported by an ultra-structural level analysis. The changes in reactive oxygen species（ROS）, malonic dialdehyde（MDA）, oxidative phosphorylation（OXPHOS） system 4 subunits levels and PD-related proteins expressions（parkin, Pink1, DJ-1, α-synuclein, and Lrrk2） reverted to near normal levels（all P〈0.05）, based on the results of immune-histological and Western blotting observations. Conclusions： The neuro-protective effects of EAS are linked to protecting mice against MPTPinduced mitochondrial dysfunction and structuraldamage.Therefore,EAS is a promising candidate for the prevention or treatment of mitochondrial neurodegenerative disorders,such as PD.