Leaf Extract of Sedum kamtschaticum Fisch. & Mey. Ameliorates Cognitive Dysfunction in Trimethyltin-treated Rats
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Background: Alzheimer’s disease (AD) is a major neurodegenerative disorder and major type of dementia with progressive cognitive deficits, including multifactorial disorders. The present study examined the therapeutic effect of Sedum kamtschaticum leaf extract (SKE) on cognitive dysfunction disorder induced in rats through trimethyltin (TMT) administration. Methods and Results: In the preliminary screening experiment, SKE was selected as an acetylcholinesterase (AChE) inhibitor. Rats in the negative control and SKE groups were intraperitoneally injected with TMT (8 ㎎/㎏ body weight) dissolved in 0.9% saline and normal rats were injected with 0.9% saline alone. Doses of SKE (100, and 300 ㎎/㎏) were orally administered to the rats for 14 days. Normal and control rats were treated with saline for the same period. We performed a behavioral test using a Morris water maze and found that the escape and latency time periods of the SKE300 rats were shorter than those of the control rats. SKE therefore ameliorated cognitive dysfunction in this animal model. Immunohistochemical assay of biomarkers in the hippocampal cells revealed that the cell levels of phosphorylated cAMP response element binding protein (p-CREB) and AChE in the CA3 region of the control group were lower than those in the normal group. However, p-CREB and AChE reactive hippocampal cells in SKE300 group were significantly increased compared to those of the control. The hippocampal cells of brain-derived neurotrophic factor (BDNF) and protein kinase C (PKC) in control rats tended to be lower than the normal group, while the cells in the SKE groups tended to be higher than the control group. Conclusions: These results suggest that SKE ameliorates cognitive disorders through the neuroprotective effects related to p-CREB and AChE in the hippocampal cells.
Abstract
Background: Alzheimer’s disease (AD) is a major neurodegenerative disorder and major type of dementia with progressive cognitive deficits, including multifactorial disorders. The present study examined the therapeutic effect of Sedum kamtschaticum leaf extract (SKE) on cognitive dysfunction disorder induced in rats through trimethyltin (TMT) administration. Methods and Results: In the preliminary screening experiment, SKE was selected as an acetylcholinesterase (AChE) inhibitor. Rats in the negative control and SKE groups were intraperitoneally injected with TMT (8 ㎎/㎏ body weight) dissolved in 0.9% saline and normal rats were injected with 0.9% saline alone. Doses of SKE (100, and 300 ㎎/㎏) were orally administered to the rats for 14 days. Normal and control rats were treated with saline for the same period. We performed a behavioral test using a Morris water maze and found that the escape and latency time periods of the SKE300 rats were shorter than those of the control rats. SKE therefore ameliorated cognitive dysfunction in this animal model. Immunohistochemical assay of biomarkers in the hippocampal cells revealed that the cell levels of phosphorylated cAMP response element binding protein (p-CREB) and AChE in the CA3 region of the control group were lower than those in the normal group. However, p-CREB and AChE reactive hippocampal cells in SKE300 group were significantly increased compared to those of the control. The hippocampal cells of brain-derived neurotrophic factor (BDNF) and protein kinase C (PKC) in control rats tended to be lower than the normal group, while the cells in the SKE groups tended to be higher than the control group. Conclusions: These results suggest that SKE ameliorates cognitive disorders through the neuroprotective effects related to p-CREB and AChE in the hippocampal cells.
참고문헌 (13)
- Chen H, "Tacrine(10)-hupyridone prevents postoperative cognitive dysfunction via the activation of BDNF pathway and the inhibition of AChE in aged mice", Frontiers in Cellular Neuroscience, 12, pp.396~ (2018)
- Čolović MB, "Molecular mechanisms associated with long-term consolidation of the NMDA signals", Life Sciences, 67, pp.335~364 (2000)
- Rinne JO, "Brain acetylcholinesterase activity in mild cognitive impairment and early alzheimer’s disease", Journal of Neurology, Neurosurgery, and Psychiatry, 74, pp.113~115 (2003)
- Sadeghi L, "Improving effects of Echium amoenum aqueous extract on rat model of alzheimer's disease", Journal of Integrative Neuroscience, 17, pp.661~669 (2018)
- Saleem U, "Experimental and computational studies to characterize and evaluate the therapeutic effect of Albizia lebbeck(L.) seeds in alzheimer’s disease", Medicina, 55, pp.184~ (2019)
- Hyun Soo Shim, "Krill-Derived Phosphatidylserine Improves TMT-Induced Memory Impairment in the Rat", Biomolecules & Therapeutics, 20(2), pp.207~213 (2012), 한국응용약물학회
- Singhal G, "Inflammasomes in neuroinflammation and changes in brain function: A focused review", Frontiers in Neuroscience, 8, pp.315~ (2014)
- Tabet N, "Acetylcholinesterase inhibitors for alzheimer’s disease : Anti-inflammatories in acetylcholine clothing", Age and Ageing, 35, pp.336~338 (2006)
- Talesa VN, "Acetylcholinesterase in alzheimer’s disease", Mechanisms of Ageing and Development, 122, pp.1961~1969 (2001)
- West MJ, "Differences in the pattern of hippocampal neuronal loss in normal ageing and alzheimer's disease", The Lancet, 344, pp.769~772 (1994)
- Ye MS, "Neuroprotective effect of bean phosphatidylserine on TMTinduced memory deficits in a rat model", International Journal of Molecular Sciences, 21, pp.4901~ (2020)[DOI]
- Ye MS, "Neuroprotective effects of Cuscutae semen in a mouse model of Parkinson’s disease", Evidence-Based Complementary and Alternative Medicine, 2014, pp.150153~ (2014)[DOI]
- Zhang C, "Prenatal deltamethrin exposure-induced cognitive impairment in offspring is ameliorated by memantine through NMDAR", BDNF signaling in hippocampus, 2018, pp.12, 615~