Journal
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
Volume 21, Issue 4, Pages 367-374Publisher
BENTHAM SCIENCE PUBL
DOI: 10.2174/1871527320666210827112609
Keywords
Scutellaria baicalensis georgi; flavonoids; Alzheimer's disease; tau protein; hyperphosphorylation; neurofibrillary tangles (NFTs)
Categories
Funding
- Hebei Provin-cial Natural Science Foundation [C2009001007, H2014406048, H2019406063]
- Hebei Provincial Administra-tion of Traditional Chinese Medicine [05027, 2014062]
- Hebei Provincial Education Department [ZD20131022, ZD2019057]
- Hebei Provincial Hundred Outstanding Inno-vated Talents (First Batch)
- Key Subject Construction Pro-ject of Hebei Provincial College
- Technology Innovation Guidance Project-Science and Technology Work Confer-ence of Hebei Provincial Department of Science and Tech-nology
- Key Subject Construction Project of Pharmacol-ogy of Traditional Chinese Medicine of Hebei Provincial Traditional Chinese Medicine [[2021] 12]
- Key De-velopment Subject of Pharmacology of Traditional Chinese Medicine of Chengde Medical College [[2020] 49]
- Science and Technology Innovation Team Construction Pro-ject of Chengde Medical College of China [[2020] 50]
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This study demonstrates that flavonoids from Scutellaria baicalensis Georgi (SSF) can reduce hyperphosphorylation of Tau protein in the brain, improving memory impairment in rats with Alzheimer's Disease (AD).
Background: Neurofibrillary Tangles (NFTs), formed by hyperphosphorylation of Tau protein in Alzheimer's Disease (AD), arethe main pathomechanisms of neuronal degeneration, which indicate a sign of brain disorder. NFTs are positively correlated with the degree of cognitive impairment in AD. Objective: The objective of this study isto investigate the effect of flavonoids from the stems and leaves of Scutellaria baicalensis Georgi (SSF) on the hyperphosphorylated expression levels at multiple sites of Tau protein induced by beta-amyloid protein 25-35 (A beta(25-35)) in combination with aluminum trichloride (AlCl3) and recombinant human transforming growth factor-beta 1(RHTGF-beta 1) (composited A beta) in rats. Methods: The AD rat models were established by intracerebroventricular injection of A beta(25-35) and AlCl3 combined with RHTGF-beta(1). On day 45, after the operation, the Morris water maze test was conducted to screen the memory impairment of AD models. The successful model rats were randomly divided into the model group and the three-dose drug group. The drug group rats were orally administered SSF daily for 38 days. Western blotting was performed to detect the protein expression of P-Tau (Thr 181), P-Tau (Thr 217), P-Tau (Thr 231), P-Tau (Ser 199), P-Tau (Ser 235), P -Tau (Ser 396), and P-Tau (Ser 404) in the hippocampus and cerebral cortex of rats. Results: Compared with the sham group, the expression of P-Tau (Thr 181), P-Tau (Thr 217), P -Tau (Thr 231), P-Tau (Ser 199), P-Tau (Ser 235), P-Tau (Ser 396), and P-Tau (Ser 404)was significantly increased in the hippocampus and cerebral cortex of the model group (P < 0.01). However, the three doses of SSF, i.e., 35, 70, and 140 mg/kg, regulated the expression of phosphorylated Tau proteinto varying degrees in the hippocampus and cerebral cortex of AD model rats (P < 0.01). Conclusion: SSF could significantly reduce the protein expression levels of P-Tau (Thr 181), P Tau (Thr 217), P-Tau (Thr 231), P-Tau (Ser 199), P-Tau (Ser 235), P-Tau (Ser 396), and P-Tau (Ser 404), induced by the intracerebroventricular injection of composited A beta, in rats' brain. These results indicated that the neuro-protection and the improvement in the impaired memory of rats by SSF were due to the inhibition of hyperphosphorylation of Tau protein at multiple sites in rats' brain.
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