Acceleration of the meckel syndrome by near-infrared light therapy.
Acceleration of the meckel syndrome by near-infrared light therapy.
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近红外光疗法加速梅克尔综合征。
DOI：
10.1159/000332046
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发表时间：
2011
期刊：
影响因子：
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通讯作者：
Henshel,DianeS
中科院分区：
文献类型：
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作者：
Lim,Jinhwan;Gattone2nd,VincentH;Sinders,Rachel;Miller,CarolineA;Liang,Yun;Harris,Peter;Watkins3rd,JohnB;Henshel,DianeS
背景/目的：使用窄带近红外（NIR）光（使用发光二极管，LED）的光疗被用于治疗某些医疗状况。这种窄带红光已被证明可以刺激线粒体中的细胞色素c氧化酶（CCO），从而刺激ATP的产生，并具有刺激伤口愈合的能力。LED处理还降低了测试系统中化学诱导的氧化应激。由于已知肾脏囊性疾病存在氧化应激和抗氧化保护降低的证据，因此我们假设近红外光疗法可能会改善肾脏囊性疾病的肾脏病理。方法：患有梅克尔综合征（MKS）的Wistar-Wpk/Wpk大鼠在第10 - 18天接受光疗法，此时评估疾病严重程度。Wpk大鼠每天用窄带红光（640 - 690 nm波长）治疗80 s或假治疗。在处死时，评价肾脏和脑病理学，并评估肾脏表达和酶活性以评价氧化应激。收集血液进行血尿素氮（BUN）测定，左肾冷冻生化评价，右肾和头部固定的形态evaluation.Results：有没有显着影响的LED治疗体重（BW）或肾脏总重量在非囊性大鼠。囊性与非囊性对照组相比，肾脏总重量增加，无肾BW降低。与非光处理的囊性大鼠（对照）相比，LED降低了囊性大鼠的BW和总肾脏重量。与对照组大鼠相比，囊性大鼠的BUN已增加近6倍。与囊性和对照大鼠相比，非囊性和囊性大鼠中的BUN在NIR处理下进一步增加近2倍。与Wpk/Wpk（脑室体积表示为总体积和无肾BW的百分比）相关的脑积水在NIR治疗的囊性大鼠中也比正常对照大鼠更严重。肾脏谷胱甘肽过氧化物酶和过氧化氢酶（CAT）减少，而超氧化物歧化酶和CCO增加。与正常对照组大鼠相比，NIR增加了CAT和CCO，略微降低了谷胱甘肽S-转移酶和谷胱甘肽还原酶。NIR的有害作用可能与囊性病变进展相关的肾血流量减少有关。压缩囊肿可能不允许足够的氧气或营养供应，以支持增加的氧化磷酸化相关的细胞活性，和增加的需求引起的NIR增加CCO可能会产生进一步的氧化stress.Conclusion：LED光疗开始后，症状的发作是有害的MKS诱导的病理。NIR刺激CCO，从而增加肾脏对氧气的需求。我们推测，囊性压迫的血管损害氧的可用性和增强CCO活性产生更多的自由基，这是不充分解毒的增加CAT活性。
Background/Aims:Phototherapy using a narrow-band, near-infrared (NIR) light (using a light-emitting diode, LED) is being used to treat certain medical conditions. This narrow-band red light has been shown to stimulate cytochrome c oxidase (CCO) in mitochondria that would stimulate ATP production and has the ability to stimulate wound healing. LED treatment also decreases chemical-induced oxidative stress in tested systems. As renal cystic diseases are known to have evidence of oxidative stress with reduced antioxidant protection, we hypothesized that NIR light therapy might ameliorate the renal pathology in renal cystic disease.Methods:Wistar-Wpk/Wpk rats with Meckel syndrome (MKS) were treated with light therapy on days 10–18 at which time disease severity was evaluated. Wpk rats were either treated daily for 80 s with narrow-band red light (640–690 nm wavelength) or sham treated. At termination, renal and cerebral pathology was evaluated, and renal expression and activity of enzymes were assessed to evaluate oxidative stress. Blood was collected for blood urea nitrogen (BUN) determination, the left kidney frozen for biochemical evaluation, and the right kidney and head fixed for morphological evaluation.Results:There were no significant effects of LED treatment on body weight (BW) or total kidney weight in non-cystic rats. Total kidney weight was increased and anephric BW was decreased in cystic versus non-cystic controls. LED reduced BW and total kidney weight in cystic rats compared to non-light-treated cystic (control) rats. BUN was already increased almost 6-fold in cystic rats compared to control rats. BUN was further increased almost 2-fold with NIR treatment in both non-cystic and cystic rats compared to cystic and control rats. The hydrocephalus associated with Wpk/Wpk (ventricular volume expressed as total volume and as percent of anephric BW) was also more severe in NIR-treated cystic rats compared to the normal control rats. Renal glutathione peroxidase and catalase (CAT) were reduced in the cystic kidney while superoxide dismutase and CCO were increased. NIR increased CAT and CCO, marginally decreased glutathione S-transferase and slightly decreased glutathione reductase in cystic rats compared to the normal control rats. The detrimental effects of NIR may be related to reduced renal blood flow associated with progression of cystic pathology. Compression by cysts may not allow sufficient oxygen or nutrient supply necessary to support the increased oxidative phosphorylation-associated cellular activity, and the increased demand induced by NIR-increased CCO may have created further oxidative stress.Conclusion:LED phototherapy initiated after the onset of symptoms was detrimental to MKS-induced pathology. NIR stimulates CCO thereby increasing the kidney’s need for oxygen. We hypothesize that cystic compression of the vasculature impairs oxygen availability and the enhanced CCO activity produces more radicals, which are not sufficiently detoxified by the increased CAT activity.