Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression

Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion. This study was designed to test whether vitamin D therapy improves intestinal dysfunction in cirrhosis. Rats were subcutaneously injected with 50% sterile CCl₄ (a mixture of pure CCl₄ and olive oil, 0.3 mL/100 g) twice a week for 6 weeks. Next, 1,25(OH)₂D₃(0.5 µg/100 g) and the vehicle were administered simultaneously with CCl₄ to compare the extent of intestinal histologic damage, tight junction protein expression, intestinal barrier function, BT, intestinal proliferation, apoptosis, and enterocyte turnover. Intestinal heme oxygenase-1 (HO-1) expression and oxidative stress were also assessed. We found that vitamin D could maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, and prevent BT and intestinal barrier dysfunction. These were achieved partly through restoration of HO-1 and inhibition of oxidative stress. Taken together, our results suggest that vitamin D ameliorated intestinal epithelial turnover and improved the integrity and function of intestinal barrier in CCl₄-induced liver cirrhotic rats. HO-1 signaling activation was involved in these above beneficial effects.

Electrophysiological study of 16 patients with severe N-hexane neuropathy / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe electrophysiological changes of severe N-hexane neuropathy getting active therapies and discuss its prognosis.</p><p><b>METHODS</b>A follow-up study involved 16 adult severe N-hexane neuropathy patients who got active therapies was performed. EMG in right muscle of thenar, tibial muscle, and vastus medialis, NCV in right median nerve, common peroneal nerve, and sural nerve were determined and analyzed before treatment and in the first, the third, the ninth, and the twenty-fourth month after treatment.</p><p><b>RESULTS</b>The electrophysiology in severe N-hexane neuropathy patients showed that the voluntary potential during muscle relaxation increased by 25.0%; the motor unit potential time limit prolonged by 20.8%, and the amplitude increased by 12.5%, and multiphasic wave increased by 16.5% during mild contraction; the raise decreased by 25.0% during strong contraction. In control group, the MCV, SCV, SNAP, DML, and CMAP of median nerve were (54.63 +/- 5.33) m/s, (59.25 +/- 6.45) m/s, (26.53 +/- 6.32) microV, (3.96 +/- 0.65)ms, and (9.89 +/- 2.30) mV respectively, the MCV, CMAP, DML of common peroneal nerve were (48.49 +/- 3.25) m/s, (5.47 +/- 1.77) mV, (5.20 +/- 1.27) ms respectively, and the SCV, SNAP of sural nerve were (63.21 +/- 9.30) m/s, (4.63 +/- 1.29) microV respectively. Severe N-hexane neuropathy patients presented significantly different abnormalities in the NCV and EMG (P < 0.01). The MCV, SCV, SNAP, DML, CMAP of median nerve were (46.00 +/- 4.32) m/s, (40.66 +/- 2.65) m/s, (7.98 +/- 1.05) microV, (4.28 +/- 0.63) ms, and (6.32 +/- 1.54) mV respectively. The MCV, CMAP, DML of common peroneal nerve were (48.49 +/- 3.25) m/s, (3.21 +/- 1.99) mV, (7.32 +/- 1.65) ms respectively. The SCV, SNAP of sural nerve were (36.48 +/- 5.20) m/s, (2.15 +/- 1.22) microV respectively. These parameters gradually recovered to normal levels in 24 months after treatment.</p><p><b>CONCLUSION</b>The electrophysiological abnormalities in severe N-hexane neuropathy patients can restore after treatment, and clinical prognosis is good.</p>