lignans and Lymphoma--B-Cell

Honokiol can reduce the MI/RI-induced cTnT and CK-MB levels, apoptosis index, and mitochondrial swelling in cardiomyocytes via activating the PI3K/AKT signaling pathway.. Honokiol provides cardiac protection from MI/RI by suppressing mitochondrial apoptosis through the PI3K/AKT signaling pathway.

Topics: Animals; Apoptosis; Biphenyl Compounds; Humans; Leukemia; Lignans; Lymphoma, B-Cell; Male; Mice; Mice, Inbred C57BL; Myocardial Reperfusion Injury; Myocytes, Cardiac; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Signal Transduction

Since the increasing smoking rate among women has resulted in higher rates of embryonic malformations, it is important to search for an efficient and inexpensive agent that can help reduce the rate of serious fetal anomalies caused by maternal cigarette smoking. In this study, the bioavailability of 4-O-methylhonokiol isolated from Magnolia officinalis was first demonstrated in the mouse embryos exposed to nicotine using a whole embryo culture system.. Mouse embryos on embryonic day 8.5 were cultured with 1 mM nicotine and/or 4-O-methylhonokiol (1 × 10(-4) or 1 × 10(-3) μM) for 48 hr and were analyzed on the viewpoints of embryo developmental changes, oxidative damages, and apoptotic and inflammatory changes.. Embryos exposed to 1 mM nicotine developed not only severe morphological anomalies, increased expressions of tumor necrosis factor-α, interleukin-1β, and caspase 3 mRNAs; and elevated levels of lipid peroxidation, but also decreased levels of cytoplasmic superoxide dismutase, cytosolic glutathione peroxidase, phospholipid hydroperoxide glutathione peroxidase, hypoxia inducible factor-1α, and B-cell lymphoma-extra large mRNAs, and reduced superoxide dismutase activity. However, these parameters were significantly improved when embryos exposed to the nicotine were concurrently treated with 4-O-methylhonokiol (1 × 10(-4) or 1 × 10(-3) μM).. These findings indicate that 4-O-methylhonokiol reduces serious embryo anomalies caused by nicotine in mouse embryos via the modulations of oxidative stress, apoptosis, and inflammation, suggesting that 4-O-methylhonokiol may be a preventive and therapeutic agent against the dysmorphology induced by maternal smoking during pregnancy.

Topics: Animals; Apoptosis; Biphenyl Compounds; Caspase 3; Embryo Culture Techniques; Female; Glutathione Peroxidase; Hypoxia-Inducible Factor 1, alpha Subunit; Inflammation; Interleukin-1beta; Lignans; Lipid Peroxidation; Lymphoma, B-Cell; Male; Mice; Mice, Inbred ICR; Nicotine; Organogenesis; Oxidative Stress; Phospholipid Hydroperoxide Glutathione Peroxidase; Pregnancy; Rats; Rats, Sprague-Dawley; RNA, Messenger; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Highly oxidized lignans produced during the cytochrome P-450 metabolism in the cells show biological activities significantly different from those of their parent natural compounds. Lignans precursors of mammalian enterolignans were treated with a methyltrioxorhenium/hydrogen peroxide catalytic system to afford new compounds oxidized at benzylic as well as in arylic positions. The evaluation of the antioxidant and apoptogenic activity by in vivo protocols of these compounds showed some interesting structure-activity relationships related to the oxidation degree of the molecules.

Topics: Antioxidants; Apoptosis; Catalysis; Cell Line, Tumor; Humans; Hydrogen Peroxide; Lignans; Lymphoma, B-Cell; Organometallic Compounds; Oxidation-Reduction; Structure-Activity Relationship