Transient receptor potential V1 modulates neuroinflammation in Parkinson’s disease dementia: Molecular implications for electroacupuncture and rivastigmine | ||
| Iranian Journal of Basic Medical Sciences | ||
| دوره 24، شماره 10، دی 2021، صفحه 1336-1345 اصل مقاله (1.22 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2021.56156.12531 | ||
| نویسندگان | ||
| Sheng-Ta Tsai1، 2، 3؛ Tzu-Hsuan Wei4؛ Yu-Wan Yang1، 5؛ Ming-Kuei Lu1، 3، 5؛ Shao San6؛ Chon-Haw Tsai1، 3، 5؛ Yi-Wen Lin* 2، 7 | ||
| 1Department of Neurology, China Medical University Hospital, Taichung, Taiwan | ||
| 2Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan | ||
| 3Everflourish Neuroscience and Brain Disease Center, China Medical University Hospital, Taichung, Taiwan | ||
| 4Department of Chinese Medicine, China Medical University Hospital, Taichung, Taiwan | ||
| 5College of Medicine, China Medical University, Taichung, Taiwan | ||
| 6Department of Psychiatry, Taoyuan Psychiatric Center, Ministry of Health and Welfare, Taoyuan, Taiwan | ||
| 7Chinese Medicine Research Center, China Medical University, Taichung, Taiwan | ||
| چکیده | ||
| Objective(s): Parkinson’s disease (PD) is a common progressive neurodegeneration disease. Its incidence increases with age and affects about 1% of people over 60. Incidentally, transient receptor potential V1 (TRPV1) and its relation with neuroinflammation in mouse brain has been widely reported. Materials and Methods: We used 6-hydroxydopamine (6-OHDA) to induce PDD in mice. We then used the Morris water maze and Bio-Plex to test learning and inflammatory mediators in mouse plasma. Western blotting and immunostaining were used to examine TRPV1 pathway in the hippocampus and medial prefrontal cortex (mPFC). Results: On acquisition days 3 (Control = 4.40 ± 0.8 sec, PDD = 9.82 ± 1.52 sec, EA = 5.04 ± 0.58 sec, Riva = 4.75 ± 0.87 sec; P=0.001) and 4, reversal learning days 1, 2, 3 (Control = 2.86 ± 0.46 sec, PDD = 9.80 ± 1.83 sec, EA = 4.6 ± 0.82 sec, Riva = 4.6 ± 1.03 sec; P=0.001) and 4, PDD mice showed significantly longer escape latency than the other three groups. Results showed that several cytokines were up-regulated in PDD mice and reversed by EA and rivastigmine. TRPV1 and downstream molecules were up-regulated in PDD mice and further reversed by EA and rivastigmine. Interestingly, α7 nicotinic receptors and parvalbumin levels in both the hippocampus and prefrontal cortex increased in EA-treated mice, but not in rivastigmine-treated mice. Conclusion: Our results showed that TRPV1 played a role in the modulation of neuroinflammation of PDD, and could potentially be a new target for treatment. | ||
| کلیدواژهها | ||
| Electroacupuncture؛ Hippocampus؛ Neuroinflammation؛ Parkinson’s disease dementia؛ Rivastigmine؛ Transient receptor potential V1 | ||
| مراجع | ||
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