Attenuation of silica-induced pulmonary fibroblasts proliferation by taurine and niacin in vitro.

The objective of this study was to investigate potential role of taurine and niacin supplementation, and their combination, in an in vitro model of silica-induced, macrophage-mediated pulmonary fibroblast proliferation. Human monocytic cell line (THP-1 cell) was primed to differentiation into macrophages by phorbol myristate acetate (PMA). PMA-primed THP-1 cells were subjected to silicon dioxide exposure. Other PMA-primed THP-1 cells incubated with taurine and niacin concentration gradients, respectively, and then were treated with silicon dioxide for 6 hours. Collected THP-1 supernatants preconditioned with taurine and niacin gradients were added to human pulmonary WI-38 cells to evaluate proliferative activity. Transforming growth factor (TGF)-beta1 mRNA in macrophages and protein level in supernatant were determined by reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Taurine- and niacin-preconditioned macrophages were more resistant to silica-induced TGF-beta1 up-regulation than macrophages without precondition. Furthermore, medium conditioned with supernatant from silica-exposed macrophages following taurine and niacin pretreatment could facilitate inhibition of pulmonary fibroblast proliferation. Moreover, the above effects could be accentuated by the combination of taurine and niacin. Down-regulation of TGF-beta 1 expression in macrophages by taurine and niacin could attenuate silica-induced pulmonary fibroblasts proliferation in vitro, which may be of therapeutic potential for early stage silicosis.

Enhancement of endogenous defenses against ROS by supra-nutritional level of selenium is more safe and effective than antioxidant supplementation in reducing hypertensive target organ damage.

Hypertension-induced target organ damage (TOD), is one of the leading causes of morbidity and mortality. Reactive oxygen species (ROS) play an important role in the pathogenesis and development of hypertension. It has been suggested that hypertension-induced TOD is related to the level of oxidative stress, but is in part independent of the level of blood pressure. Therefore, in addition to anti-hypertensive drug therapy, novel strategies against ROS, will provide additional benefits to patient with hypertension. Vitamin E has long been supplemented as an effective antioxidant. However, the potential hazardous effects of vitamin E supplementation as antioxidant revealed by recent studies make its clinical and routine use prudent. Therefore, novel approaches capable of enhancing endogenous system to defend against ROS are required. Here, we propose that enhancement of intrinsic defenses against ROS by supra-nutritional level of selenium is more safe and effective than antioxidant supplementation in reducing hypertensive target organ damage, owing to its role in activating and constitution of native vital proteins and/or enzymes against oxidative stress, and the fact that scarcity of selenium can not be supplemented by normal food, and potentially extra benefits by supra-normal intake.