Previous studies demonstrated nicotine released protons from adrenergic nerves via stimulation of nicotinic acetylcholine receptors and activated transient receptor potential vanilloid-1 receptors (TRPV1) located on CGRP-containing vasodilator (CGRPergic) nerves, resulting in vasodilation. The present study investigated whether perivascular nerves release protons, which modulate axon-axonal neurotransmission.
Differences in molecular interaction between bases (adenine (A), guanine (G), and cytosine (C)) and the methyl (Me)-radical were investigated by perturbation analysis using the quantum chemical method. Part of the source of damage to the DNA was elucidated at the molecular level. In the reaction of each of the saccharide derivatives (dA, dG, and dC) with Me-radical, the reactivity of dG (?dA) is more than about 10 times larger than that of dC. Therefore, it is expected that the base G (and A) was more than about 10 times than the base C in radical-reactivity of the base. For the reaction of dA and dG with the radical, the C(8) site of the partial purine ring of dA and dG, and the C(5) site of the pyrimidine ring of dC were the main reaction sites for methylation. In the reaction of DNA composed of hydrogen-bonded base pairs G-C and A-T with the radical, the purine ring in the constituent base G reacted preferentially with the radical to yield 8-methyl-guanines.
We studied the influence of novel supramolecular substance,  rotaxane (TRO-A0001), on caspase signaling and cell viability in cancer cell lines. TRO-A0001 suppressed concentration-dependently cell proliferation. Expression of the cleaved-form caspase-3 and PARP was significantly increased in cells exposed to TRO-A0001. The expression of Bax was increased by TRO-A0001. Furthermore, the down-regulation of Bax by siRNA resulted in growth activation significantly. The morphological analysis demonstrated that TRO-A0001 increased the levels of apoptotic cells in human cancer cell lines. These results suggest that TRO-A0001 induces apoptosis in cancer cells and holds potential as a new anti-tumor medicine.
Cancer is the most common cause of death in Japan. Fundamental and clinical studies on cancer were conducted from the viewpoint of Western medicine so far. However, a sustained complete remission has not been achieved yet. In order to alleviate the side effects of anticancer drugs, some traditional herbal medicines (Kampo medicines) have been prescribed to cancer patients. We have been studying on antitumor substances in medicinal herbs and found an antitumor medicinal herb named Rhus verniciflua (lacquer, Urushi in Japanese). To investigate the antitumor effect in vitro, a plant extract mixture was prepared from six medicinal herbs containing lacquer. The plant extract mixture containing lacquer (Rv-PEM) inhibited the proliferation of several mouse and human tumor cell lines. Rv-PEM had more potent inhibitory effect on the proliferation of human leukemia cell lines (MOLT-3, KG-1) than on other tumor cell lines. The IC50 values of Rv-PEM on MOLT-3 and KG-1 cells were 0.208 and 0.293 mg/mL, respectively. After treating Rv-PEM to the tumor cells, DNA fragmentation and Caspase-3 and -9 activity increased in the treated cells. The mechanisms of the inhibitory proliferation activity of Rv-PEM would involve apoptosis of human leukemia cells (MOLT-3, KG-1, K-562) by the mitochondrial pathway.
Combinations of caffeine with L-arginine or with taurine can enhance the effect of caffeine, but the mechanisms remain elusive. This study was designed to test the hypothesis that stimulant effects of central nervous system nitric oxide (NO) may explain the beneficial effect of caffeine on combinations with amino acid, L-arginine or taurine. Caffeine increased the spontaneous locomotor activity dose-dependently (2-10 mg/kg) in mice. The locomotor activity induced by caffeine at a dose of 2 mg/kg was enhanced by combined administration of L-arginine at a dose of 600 mg/kg, or taurine at a dose of 400 mg/kg, respectively. For both combinations, enhancement was significantly inhibited by pretreatment with N-nitro-L-arginine methyl ester (L-NAME) at a dose of 40 mg/kg. These results suggest that the enhancement induced by combining caffeine with amino acid might be regulated at least in part by NO in the central nervous system.
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