Korean mistletoe (Viscum album coloratum) extract regulates gene expression related to muscle atrophy and muscle hypertrophy.

BACKGROUND: Korean mistletoe (Viscum album coloratum) is a semi-parasitic plant that grows on various trees and has a diverse range of effects on biological functions, being implicated in having anti-tumor, immunostimulatory, anti-diabetic, and anti-obesity properties. Recently, we also reported that Korean mistletoe extract (KME) improves endurance exercise in mice, suggesting its beneficial roles in enhancing the capacity of skeletal muscle. METHODS: We examined the expression pattern of several genes concerned with muscle physiology in C2C12 myotubes cells to identify whether KME inhibits muscle atrophy or promotes muscle hypertrophy. We also investigated these effects of KME in denervated mice model. RESULTS: Interestingly, KME induced the mRNA expression of SREBP-1c, PGC-1α, and GLUT4, known positive regulators of muscle hypertrophy, in C2C12 cells. On the contrary, KME reduced the expression of Atrogin-1, which is directly involved in the induction of muscle atrophy. In animal models, KME mitigated the decrease of muscle weight in denervated mice. The expression of Atrogin-1 was also diminished in those mice. Moreover, KME enhanced the grip strength and muscle weight in long-term feeding mice. CONCLUSIONS: Our results suggest that KME has beneficial effects on muscle atrophy and muscle hypertrophy.

Black rice extract protected HepG2 cells from oxidative stress-induced cell death via ERK1/2 and Akt activation.

BACKGROUND/OBJECTIVES: The objective of this study was to evaluate the protective effect of black rice extract (BRE) on tert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. MATERIALS/METHODS: Methanolic extract from black rice was evaluated for the protective effect on TBHP-induced oxidative injury in HepG2 cells. Several biomarkers that modulate cell survival and death including reactive oxygen species (ROS), caspase-3 activity, and related cellular kinases were determined. RESULTS: TBHP induced cell death and apoptosis by a rapid increase in ROS generation and caspase-3 activity. Moreover, TBHP-induced oxidative stress resulted in a transient ERK1/2 activation and a sustained increase of JNK1/2 activation. While, BRE pretreatment protects the cells against oxidative stress by reducing cell death, caspase-3 activity, and ROS generation and also by preventing ERKs deactivation and the prolonged JNKs activation. Moreover, pretreatment of BRE increased the activation of ERKs and Akt which are pro-survival signal proteins. However, this effect was blunted in the presence of ERKs and Akt inhibitors. CONCLUSIONS: These results suggest that activation of ERKs and Akt pathway might be involved in the cytoprotective effect of BRE against oxidative stress. Our findings provide new insights into the cytoprotective effects and its possible mechanism of black rice against oxidative stress.

A tocotrienol-rich fraction from grape seeds inhibits oxidative stress induced by tert-butyl hydroperoxide in HepG2 cells.

We evaluated the protective effect of a tocotrienol-rich fraction (TRF) from grape seeds on tert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. Generation of cellular reactive oxygen species (ROS), concentrations of cellular lipid peroxidation products and reduced glutathione, and antioxidant enzyme activity were used as biomarkers of cellular oxidative status. Cells pretreated with TRF (10­500 µg/mL) showed an increased resistance to oxidative stress in a dose-dependent manner, as revealed by a higher percentage of surviving cells compared to control cells. Pretreatment with TRF (5­100 µg/mL) prevented the decrease in reduced glutathione and the increase in malondialdehyde and ROS evoked by TBHP in HepG2 cells. Moreover, TRF pretreatment prevented a significant increase in glutathione peroxidase, catalase, and superoxide dismutase activities induced by TBHP. These results show that TRF has significant protective ability against TBHP-induced oxidative insult and that the modulation of antioxidant enzymes by TRF may have an important antioxidant effect on HepG2 cells.