The relationship between thiamin, folic acid and cognitive function in a rat model of uremia
End-stage renal disease is a worldwide health burden, but the pathogenesis of uremia-associated cognitive impairment (CI) is poorly recognized. We hypothesized that uremia brings about deficiency of thiamin and folic acid and causes CI by inducing oxidative stress. Therefore, 24 Sprague-Dawley rats...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | Renal Failure |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/0886022X.2024.2329257 |
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| author | Yifei Lu Chenqi Xu Kewei Xie Bingru Zhao Minzhou Wang Cheng Qian Xuemei Chen Leyi Gu Wangshu Wu Renhua Lu |
| author_facet | Yifei Lu Chenqi Xu Kewei Xie Bingru Zhao Minzhou Wang Cheng Qian Xuemei Chen Leyi Gu Wangshu Wu Renhua Lu |
| author_sort | Yifei Lu |
| collection | DOAJ |
| description | End-stage renal disease is a worldwide health burden, but the pathogenesis of uremia-associated cognitive impairment (CI) is poorly recognized. We hypothesized that uremia brings about deficiency of thiamin and folic acid and causes CI by inducing oxidative stress. Therefore, 24 Sprague-Dawley rats were randomly divided into two groups: a 5/6 nephrectomy group (n = 12) and a sham-operated group (n = 12). The Morris water maze was used to assess the cognitive function eight weeks post-surgery, and serum levels of thiamin, folic acid and homocysteine were detected subsequently. Brain and kidney tissues were collected for pathological examination and 8-Hydroxy-2’-deoxyguanosine (8-OHdG) immunochemistry staining. Results showed that the escape latency on training days 1-2 was longer, and the time in quadrant IV on experimental day 6 was significantly shorter in 5/6 nephrectomy group. Meanwhile, the uremic rats showed decreased thiamin, folic acid and increased homocysteine. We also found the time in quadrant IV was positively correlated with thiamin and folic acid level, while negatively correlated with the blood urea nitrogen and 8-OHdG positive cell proportion. Furthermore, in 5/6 nephrectomy group, the hippocampal neuron count was significantly reduced, and a greater proportion of 8-OHdG positive cells were detected. Pretreating LPS-stimulated rat microglial cells with thiamin or folic acid in vitro alleviated the inflammatory impairment in terms of cell viability and oxidative stress. In summary, we applied a uremic rat model and proved that uremia causes serum thiamin and folic acid deficiency, homocysteine elevation, along with neuron reduction and severe oxidative stress in hippocampus, finally leading to CI. |
| format | Article |
| id | doaj-art-bbdfd816fcdf456cb1911020f805ac12 |
| institution | Kabale University |
| issn | 0886-022X 1525-6049 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Renal Failure |
| spelling | doaj-art-bbdfd816fcdf456cb1911020f805ac122025-01-23T04:17:48ZengTaylor & Francis GroupRenal Failure0886-022X1525-60492024-12-0146110.1080/0886022X.2024.2329257The relationship between thiamin, folic acid and cognitive function in a rat model of uremiaYifei Lu0Chenqi Xu1Kewei Xie2Bingru Zhao3Minzhou Wang4Cheng Qian5Xuemei Chen6Leyi Gu7Wangshu Wu8Renhua Lu9Department of Pharmacy, Shanghai University of Traditional Chinese Medicine, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Anesthesiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaEnd-stage renal disease is a worldwide health burden, but the pathogenesis of uremia-associated cognitive impairment (CI) is poorly recognized. We hypothesized that uremia brings about deficiency of thiamin and folic acid and causes CI by inducing oxidative stress. Therefore, 24 Sprague-Dawley rats were randomly divided into two groups: a 5/6 nephrectomy group (n = 12) and a sham-operated group (n = 12). The Morris water maze was used to assess the cognitive function eight weeks post-surgery, and serum levels of thiamin, folic acid and homocysteine were detected subsequently. Brain and kidney tissues were collected for pathological examination and 8-Hydroxy-2’-deoxyguanosine (8-OHdG) immunochemistry staining. Results showed that the escape latency on training days 1-2 was longer, and the time in quadrant IV on experimental day 6 was significantly shorter in 5/6 nephrectomy group. Meanwhile, the uremic rats showed decreased thiamin, folic acid and increased homocysteine. We also found the time in quadrant IV was positively correlated with thiamin and folic acid level, while negatively correlated with the blood urea nitrogen and 8-OHdG positive cell proportion. Furthermore, in 5/6 nephrectomy group, the hippocampal neuron count was significantly reduced, and a greater proportion of 8-OHdG positive cells were detected. Pretreating LPS-stimulated rat microglial cells with thiamin or folic acid in vitro alleviated the inflammatory impairment in terms of cell viability and oxidative stress. In summary, we applied a uremic rat model and proved that uremia causes serum thiamin and folic acid deficiency, homocysteine elevation, along with neuron reduction and severe oxidative stress in hippocampus, finally leading to CI.https://www.tandfonline.com/doi/10.1080/0886022X.2024.2329257End-stage renal diseaseuremic rat modelcognitive impairmentvitamin Boxidative stress |
| spellingShingle | Yifei Lu Chenqi Xu Kewei Xie Bingru Zhao Minzhou Wang Cheng Qian Xuemei Chen Leyi Gu Wangshu Wu Renhua Lu The relationship between thiamin, folic acid and cognitive function in a rat model of uremia Renal Failure End-stage renal disease uremic rat model cognitive impairment vitamin B oxidative stress |
| title | The relationship between thiamin, folic acid and cognitive function in a rat model of uremia |
| title_full | The relationship between thiamin, folic acid and cognitive function in a rat model of uremia |
| title_fullStr | The relationship between thiamin, folic acid and cognitive function in a rat model of uremia |
| title_full_unstemmed | The relationship between thiamin, folic acid and cognitive function in a rat model of uremia |
| title_short | The relationship between thiamin, folic acid and cognitive function in a rat model of uremia |
| title_sort | relationship between thiamin folic acid and cognitive function in a rat model of uremia |
| topic | End-stage renal disease uremic rat model cognitive impairment vitamin B oxidative stress |
| url | https://www.tandfonline.com/doi/10.1080/0886022X.2024.2329257 |
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