Nutritional zinc deficiency aggravates inflammation, subsequently causing anemia and splenomegaly in rats; however, the mechanism underlying such splenomegaly remains poorly understood. Therefore, in this study, we aimed to elucidate the mechanisms underlying the splenomegaly and anemia occurring in zinc-deficient rats and investigate whether these effects of zinc deficiency could be reversed by interleukin (IL)-4 administration or zinc supplementation. Five-week-old male Sprague-Dawley rats were fed a standard diet; fed a zinc-deficient diet (n = 7 each) and injected with saline or IL-4; or fed a zinc-deficient diet for 6 weeks followed by a standard diet for 4 weeks thereafter. White blood cells, segmented neutrophils, platelets, CD4+ T cells, CD11b/c+ granulocytes, CINC/GRO+ cells, and myeloperoxidase-positive cells in the blood and spleen of the zinc-deficient rats were significantly higher than those in all the other groups. Conversely, red blood cells, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, lymphocytes, and CD8+ T cells in the blood of the zinc-deficient rats were significantly lower than those in the other groups. Furthermore, serum aspartate aminotransferase, lactate dehydrogenase, indirect bilirubin concentrations, and erythrocyte osmotic fragility in the zinc-deficient rats were significantly higher than those in the other groups. Moreover, zinc deficiency significantly decreased the GATA1 protein levels in the spleen. Collectively, these results indicate that zinc deficiency aggravates the inflammatory response and causes hemolytic anemia and splenomegaly. Importantly, IL-4 administration and zinc supplementation can reverse the zinc deficiency-induced hemolytic anemia and splenomegaly.

中文翻译：

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Interleukin-4 给药或锌补充剂可有效预防缺锌引起的溶血性贫血和脾肿大。

营养性缺锌会加重炎症，继而引起大鼠贫血和脾肿大；然而，这种脾肿大的潜在机制仍然知之甚少。因此，在本研究中，我们旨在阐明缺锌大鼠脾肿大和贫血的潜在机制，并研究是否可以通过白介素 (IL)-4 给药或补锌来逆转缺锌的这些影响。给五周大的雄性 Sprague-Dawley 大鼠喂食标准饮食；喂食缺锌饮食（每种 n = 7）并注射生理盐水或 IL-4；或喂食缺锌饮食 6 周，然后再喂标准饮食 4 周。白细胞、分段中性粒细胞、血小板、CD4+ T 细胞、CD11b/c+ 粒细胞、CINC/GRO+ 细胞、缺锌大鼠血液和脾脏中髓过氧化物酶阳性细胞数显着高于其他各组。相反，缺锌大鼠血液中的红细胞、血红蛋白、血细胞比容、平均红细胞体积、平均红细胞血红蛋白、平均红细胞血红蛋白浓度、淋巴细胞和 CD8+ T 细胞显着低于其他组。此外，缺锌大鼠血清天冬氨酸氨基转移酶、乳酸脱氢酶、间接胆红素浓度和红细胞渗透脆性显着高于其他组。此外，缺锌会显着降低脾脏中的 GATA1 蛋白水平。总的来说，这些结果表明缺锌会加剧炎症反应并导致溶血性贫血和脾肿大。重要的是，IL-4 给药和锌补充剂可以逆转缺锌引起的溶血性贫血和脾肿大。