Nicotinamide Mononucleotide Protects against Retinal Dysfunction in a Murine Model of Carotid Artery Occlusion.
Nicotinamide Mononucleotide Protects against Retinal Dysfunction in a Murine Model of Carotid Artery Occlusion.
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DOI：
10.3390/ijms232314711
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发表时间：
2022-11-25
影响因子：
5.6
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中科院分区：
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心血管异常介导的视网膜缺血导致严重的视力损害。视网膜缺血涉及大量病理过程，包括氧化应激、反应性胶质增生和视网膜功能缺陷。因此，通过调节这些病理过程来维持视网膜功能可以预防或保护视力丧失。烟酰胺单核苷酸（NMN）是一种重要的烟酰胺腺嘌呤二核苷酸（NAD+）中间体，近年来已被提名为视网膜疾病的一个有前途的治疗靶点。然而，NMN的保护作用尚未在心血管疾病诱导的视网膜缺血中进行检查。在我们的研究中，我们的目的是探讨其有前途的影响，NMN在缺血视网膜的小鼠模型的颈动脉闭塞。在成年雄性C57 BL/6小鼠中进行单侧颈总动脉手术闭塞（UCCAO）后，每天向小鼠腹腔内注射NMN（500 mg/kg/天）直至实验结束。利用视网膜电图和生物分子测定来测量视网膜中的眼功能和进一步的分子改变。我们发现，UCCAO诱导的视网膜功能障碍被抑制，病理性胶质增生减少，视网膜NAD+水平得到保留，抗氧化分子（核因子红细胞-2相关因子2; Nrf 2）的表达上调连续管理NMN。我们目前的研究结果首次表明，NMN治疗有希望抑制心血管疾病介导的视网膜缺血性功能障碍。
Cardiovascular abnormality-mediated retinal ischemia causes severe visual impairment. Retinal ischemia is involved in enormous pathological processes including oxidative stress, reactive gliosis, and retinal functional deficits. Thus, maintaining retinal function by modulating those pathological processes may prevent or protect against vision loss. Over the decades, nicotinamide mononucleotide (NMN), a crucial nicotinamide adenine dinucleotide (NAD+) intermediate, has been nominated as a promising therapeutic target in retinal diseases. Nonetheless, a protective effect of NMN has not been examined in cardiovascular diseases-induced retinal ischemia. In our study, we aimed to investigate its promising effect of NMN in the ischemic retina of a murine model of carotid artery occlusion. After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments. Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina. We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN. Our present outcomes first suggest a promising NMN therapy for the suppression of cardiovascular diseases-mediated retinal ischemic dysfunction.
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影响因子：
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作者：
Lee D;Nakai A;Miwa Y;Tomita Y;Serizawa N;Katada Y;Hatanaka Y;Tsubota K;Negishi K;Kurihara T
通讯作者：
Kurihara T
影响因子：
2.7
作者：
Lee D;Jeong H;Miwa Y;Shinojima A;Katada Y;Tsubota K;Kurihara T
通讯作者：
Kurihara T
影响因子：
5.6
作者：
通讯作者：
--
影响因子：
3.4
作者：
Minhas G;Morishita R;Anand A
通讯作者：
Anand A
影响因子：
--
作者：
Kwon DH;Kim YC;Kang KT
通讯作者：
Kang KT