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[JNK/p38 MAPK involves in ginsenoside Rb1 attenuating beta-amyloid peptide (25-35) -induced tau protein
Jin-Qiu Song1, Xiao-Chun Chen, Jing Zhang
1Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, Fuzhou 350001, China.
Abstract:
To explore the effect of ginsenoside Rb1 on JNK/p38 MAPK in the process of beta-amyloid peptide (25-35) -induced tau protein hyperphosphorylation, Western blotting and immunocytochemical stain were performed to observe the tau protein phosphorylation and the expression of JNK/p38 MAPK. The level of tau protein phosphorylation in the sites of Ser396 , Ser199/202 and Thr205 increased after rat cortical neurons exposed to 20 micromol x L(-1) Abeta25-35, meanwhile the level of JNK/p38 MAPK also increased after Abeta25-35 treatment for 12 h. Pretreatment with several doses of ginsenoside Rbl markedly attenuated tau protein hyperphosphorylation and the expression of JNK/p38 MAPK. Ginsenoside Rbl markedly attenuated tau protein hyperphosphorylation through JNK/p38 MAPK pathway.
Insights
Ginsenoside Rb1 effectively reduces tau protein hyperphosphorylation, a key factor in neurodegenerative diseases. This compound works by inhibiting the JNK/p38 MAPK pathway, offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Beta-amyloid peptide (Abeta) is implicated in neurodegenerative diseases.
- Abeta induces tau protein hyperphosphorylation, a hallmark of neuronal damage.
- The JNK/p38 MAPK pathway is involved in Abeta-induced neuronal dysfunction.
Purpose of the Study:
- To investigate the effect of ginsenoside Rb1 on JNK/p38 MAPK signaling.
- To determine if ginsenoside Rb1 can prevent beta-amyloid peptide (25-35)-induced tau protein hyperphosphorylation.
Main Methods:
- Rat cortical neurons were treated with beta-amyloid peptide (25-35).
- Western blotting and immunocytochemical staining were used to assess tau phosphorylation and JNK/p38 MAPK expression.
- Neurons were pretreated with varying doses of ginsenoside Rb1.
Main Results:
- Abeta25-35 treatment increased tau protein hyperphosphorylation at specific sites (Ser396, Ser199/202, Thr205).
- Abeta25-35 also elevated the expression of JNK/p38 MAPK.
- Ginsenoside Rb1 pretreatment significantly reduced tau hyperphosphorylation and JNK/p38 MAPK levels.
Conclusions:
- Ginsenoside Rb1 demonstrates neuroprotective effects against Abeta-induced tau hyperphosphorylation.
- The protective mechanism of ginsenoside Rb1 involves the modulation of the JNK/p38 MAPK pathway.
- Ginsenoside Rb1 shows potential as a therapeutic agent for neurodegenerative conditions involving tau pathology.
