Protection from antimycin A-induced mitochondrial dysfunction by Nelumbo nucifera seed extracts.

Antimycin A (AMA) damages the mitochondria through inhibition of mitochondrial electron transport. In this study, exposure of L6 rat skeletal muscle cells to AMA induced a decrease in ATP content, followed by a decrease in mitochondrial membrane potential, leading to apoptosis. We evaluated the protective effects of water and ethanol extracts of Nelumbo nucifera seeds on L6 cells with AMA-induced oxidative stress. We found that the extracts reduced cellular apoptosis; preserved the mitochondrial membrane potential; protected mitochondrial ATP production; inhibited p53, Bax, and caspase 3 activities; and induced Bcl-2 production. Our results suggested that AMA induced apoptosis in L6 cells via impairment of mitochondrial function. N. nucifera extracts protected the cells from this mitochondria-mediated cell death.

Scutellaria baicalensis Extracts and Flavonoids Protect Rat L6 Cells from Antimycin A-Induced Mitochondrial Dysfunction.

Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species (ROS). ROS formation, aging, and reduction of mitochondrial biogenesis contribute to mitochondrial dysfunction. The present study sought to investigate extracts of Scutellaria baicalensis and its flavonoids (baicalin, baicalein, and wogonin), whether they could protect mitochondria against oxidative damage. The viability of L6 cells treated with AMA increased in the presence of flavonoids and extracts of S. baicalensis. ATP production decreased in the AMA treated group, but increased by 50% in cells treated with flavonoids (except wogonin) and extracts of S. baicalensis compared to AMA-treated group. AMA treatment caused a significant reduction (depolarized) in mitochondrial membrane potential (MMP), whereas flavonoid treatment induced a significant increase in MMP. Mitochondrial superoxide levels increased in AMA treated cells, whereas its levels decreased when cells were treated with flavonoids or extracts of S. baicalensis. L6 cells treated with flavonoids and extracts of S. baicalensis increased their levels of protein expression compared with AMA-treated cells, especially water extracts performed the highest levels of protein expression. These results suggest that the S. baicalensis extracts and flavonoids protect against AMA-induced mitochondrial dysfunction by increasing ATP production, upregulating MMP, and enhancing mitochondrial function.