The effect of long-term dehydration and subsequent rehydration on markers of inflammation, oxidative stress and apoptosis in the camel kidney.
The effect of long-term dehydration and subsequent rehydration on markers of inflammation, oxidative stress and apoptosis in the camel kidney.
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DOI：
10.1186/s12917-020-02628-5
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发表时间：
2020-11-23
影响因子：
2.6
通讯作者：
Adem A
中科院分区：
文献类型：
--
作者：
Ali MA;Abu Damir H;Ali OM;Amir N;Tariq S;Greenwood MP;Lin P;Gillard B;Murphy D;Adem A
脱水对许多物种都有有害影响，但骆驼可以忍受长时间缺水而不会严重损害健康。肾脏在水源保护中起着至关重要的作用，然而，一些报告指出脱水骆驼的肾功能测试升高。在这项工作中，我们研究了脱水和复水对肾皮质和髓质的促炎标志物，氧化应激和细胞凋亡沿着相应的基因表达的影响。细胞因子IL-1β和IL-18在脱水骆驼肾皮质中显著升高，可能由肾小管上皮细胞、足细胞和/或系膜细胞表达。再水化后IL-18持续升高。结果表明，脱水可诱导肾皮质氧化应激，表现为MDA、GSH含量显著升高，SOD、CAT含量显著降低;而在髓质，CAT含量显著降低，MDA、GSH、SOD含量无明显变化。再水化消除了氧化应激。与MDA水平的增加平行，我们观察到MDA合成途径中PTGS 1 mRNA水平的增加。GCLC mRNA的表达水平，参与GSH的合成，在肾皮质的再水化上调。然而，SOD 1和SOD 3 mRNA水平下降，与SOD活性平行，在皮层脱水。caspase 3和9、p53和PARP 1表达明显增加，表明细胞凋亡由内源性途径触发。BCL 2l 1 mRNA水平的表达，编码BCL-xL，在皮质脱水下调。CASP 3的表达水平显着增加，在髓质脱水和持续后，再水化，而TP 53的表达增加皮质再水化。caspase 8和TNF-α的变化对诱导外源性凋亡线索的影响可忽略不计。通常，细胞凋亡标记物在再水化后变化极大，表明动物在三天内没有完全恢复。脱水引起肾皮质氧化应激和皮质、髓质细胞凋亡。肾皮质和髓质在研究的所有参数中均不均匀，表明对脱水/补液的反应不同。测试参数的一些变化与稳态mRNA水平的改变直接相关。
Dehydration has deleterious effects in many species, but camels tolerate long periods of water deprivation without serious health compromise. The kidney plays crucial role in water conservation, however, some reports point to elevated kidney function tests in dehydrated camels. In this work, we investigated the effects of dehydration and rehydration on kidney cortex and medulla with respect to pro-inflammatory markers, oxidative stress and apoptosis along with corresponding gene expression. The cytokines IL-1β and IL-18 levels were significantly elevated in the kidney cortex of dehydrated camel, possibly expressed by tubular epithelium, podocytes and/or mesangial cells. Elevation of IL-18 persisted after rehydration. Dehydration induced oxidative stress in kidney cortex evident by significant increases in MDA and GSH, but significant decreases in SOD and CAT. In the medulla, CAT decreased significantly, but MDA, GSH and SOD levels were not affected. Rehydration abolished the oxidative stress. In parallel with the increased levels of MDA, we observed increased levels of PTGS1 mRNA, in MDA synthesis pathway. GCLC mRNA expression level, involved in GSH synthesis, was upregulated in kidney cortex by rehydration. However, both SOD1 and SOD3 mRNA levels dropped, in parallel with SOD activity, in the cortex by dehydration. There were significant increases in caspases 3 and 9, p53 and PARP1, indicating apoptosis was triggered by intrinsic pathway. Expression of BCL2l1 mRNA levels, encoding for BCL-xL, was down regulated by dehydration in cortex. CASP3 expression level increased significantly in medulla by dehydration and continued after rehydration whereas TP53 expression increased in cortex by rehydration. Changes in caspase 8 and TNF-α were negligible to instigate extrinsic apoptotic trail. Generally, apoptotic markers were extremely variable after rehydration indicating that animals did not fully recover within three days. Dehydration causes oxidative stress in kidney cortex and apoptosis in cortex and medulla. Kidney cortex and medulla were not homogeneous in all parameters investigated indicating different response to dehydration/rehydration. Some changes in tested parameters directly correlate with alteration in steady-state mRNA levels.
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影响因子：
--
作者：
Ayala A;Muñoz MF;Argüelles S
通讯作者：
Argüelles S
影响因子：
4.6
作者：
Hilliard, Lucinda M.;Colafella, Katrina M. Mirabito;Denton, Kate M.
通讯作者：
Denton, Kate M.
影响因子：
2.6
作者：
Ali, Mahmoud Alhaj;Kazzam, Elsadig;Adem, Abdu
通讯作者：
Adem, Abdu
影响因子：
56.9
作者：
Chipuk, JE;Bouchier-Hayes, L;Green, DR
通讯作者：
Green, DR
影响因子：
3.7
作者：
Adem, Abdu;Al Haj, Mahmoud;Kazzam, Elsadig
通讯作者：
Kazzam, Elsadig