β -胡萝卜素(维生素原A)可降低ccl4诱导的大鼠肝脏炎症和纤维化的严重程度。

W F Seifert, A Bosma, H F Hendriks, R E van Leeuwen, G C van Thiel-de Ruiter, I Seifert-Bock, D L Knook, A Brouwer
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引用次数: 61

摘要

早期的大鼠实验数据表明,视黄醇酯(维生素A)的施用强烈影响CCl4对肝脏的作用。胶原蛋白的积累受到抑制,但ccl4毒性增加,死亡率高。本研究旨在探讨β -胡萝卜素(维生素原A)对大鼠ccl4相关全身毒性和肝毒性的影响。与未服用β -胡萝卜素的大鼠肝脏相比,在ccl4治疗期间口服β -胡萝卜素导致肝脏羟脯氨酸含量显著降低,在组织病理学上,肝纤维化程度较轻。该研究还表明,β -胡萝卜素可以防止ccl4损伤肝脏中类维生素a的长期流失。与先前发现的视黄醇酯(维生素A)不同,没有观察到β -胡萝卜素的显著毒性作用。本实验研究提示-胡萝卜素具有降低肝纤维化严重程度的治疗潜力,且无明显毒性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Beta-carotene (provitamin A) decreases the severity of CCl4-induced hepatic inflammation and fibrosis in rats.

Earlier data from experiments in rats have shown that administration of retinyl esters (vitamin A) strongly influences the effects of CCl4 on the liver. The accumulation of collagen was inhibited, but an increase in CCl4-toxicity with high mortality was observed. The present study was conducted to examine the effects of beta-carotene (provitamin A) on CCl4-related general and hepatic toxicity in rats. Oral administration of beta-carotene during CCl4-treatment resulted, biochemically, in a significantly lower increase in the hydroxyproline liver content and, histopathologically, in less severe liver fibrosis as compared with the liver of rats not treated with beta-carotene. The study also showed that beta-carotene administration could prevent the long-term loss of retinoids from the CCl4-injured liver. No significant toxic effects of beta-carotene, as previously found with retinyl esters (vitamin A), were observed. This experimental study suggests that beta-carotene has the therapeutic potential to decrease the severity of liver fibrosis without marked toxicity.

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