Effect of early vitamin D supplementation on asthma and the possible mechanisms.

Asthma is a chronic inflammatory disease of the airways with variable airflow obstruction and bronchial hyper-responsiveness. It is believed that Th2-derived cytokines orchestrate the asthmatic response and the maintenance of the balance of Th1/Th2 plays a crucial role in prevention of asthma. Moreover, 1,25(OH)2D3, the biologically activate form of vitamin D, was reported with an almost opposite role in prevention and treatment of asthma. Therefore, in this study, we elucidated the evaluations of in vivo anti-asthma effects when treated with different doses of vitamin D and validated the relationship between vitamin D and asthma. Our data demonstrated that intervention with the appropriate dose of 1,25(OH)2D3 in early life could improve pulmonary function and reduce eosinophil cell infiltration in the airways of rat asthma models. However, overdose might play a detrimental effect. Its mechanism may correlate with the effect of 1,25(OH)2D3 on interleukin (IL)-4, IL-12, IL-13, interferon-γ, and ovalbumin-specific immunoglobulin E secretion and the expression of p-JAK1/p-STAT6/SOCS5.

L-carnitine protects against cyclosporine-induced pancreatic and renal injury in rats.

BACKGROUND: L-carnitine has protective effects against various types of injury. This study was designed to evaluate the beneficial effects of L-carnitine on pancreatic and renal injuries caused by cyclosporine (CsA). METHODS: Rats maintained on a low sodium diet were given vehicle (olive oil, 1 mL/kg/d), CsA (15 mg/kg/d), L-carnitine (50 or 200 mg/kg/d), or a combination of CsA and L-carnitine for 4 weeks. The impact of L-carnitine on pancreatic injury was assessed by blood glucose levels, plasma insulin concentrations, and hemoglobulin A1c (HbA1c). In addition, the protective effects of L-carnitine against CsA-induced kidney injury were evaluated in terms of renal function, histopathology (inflammatory cell influx and tubulointerstitial fibrosis), oxidative stress (8-hydroxy 2'-deoxyguanosine, 8-OHdG), transforming growth factor-betal (TGF-ß1), apoptosis (caspase-3), and autophagy (LC3-II). RESULTS: CsA treatment caused diabetes, renal dysfunction, tubulointerstitial inflammation (ED-1-positive cells), and fibrosis, which were accompanied by an increase in 8-OHdG production and upregulation of TGF-ß1, caspase-3, and LC3-II. Concomitant administration of L-carnitine increased plasma insulin concentrations, decreasing plasma glucose and HbA1c levels. In the kidney, L-carnitine induced dose-dependent improvement of renal function, inflammation, and fibrosis in parallel with suppression of the expression of TGF-ß1 and 8-OHdG. Furthermore, the administration of L-carnitine at a high dose inhibited the expression of caspase-3 and LC3-II. CONCLUSION: These findings suggest that L-carnitine has a protective effect against CsA-induced pancreatic and renal injuries.