Immunity, inflammation and disease · 2026
Reducing Neuroinflammation via Inhibition of Fibrinogen Deposition and Microglial Activation as an Underlying Mechanism of Paning I Decoction in Ameliorating Parkinson's Disease Symptoms.
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Chen Yan-Jun, Chen Jing-Wen, Xie Ming-Rong, Wang Rui-Zhen, Wan Yu-Ling, Zeng Jie, Zhong Bing-Wu, Zhou Sheng-Qiang, Liu Fang
Аннотация
BACKGROUND: Parkinson's disease (PD) is a major neurodegenerative disorder. Some patients show limited response to standard therapies, driving the need for new complementary treatments. Paning I decoction (PNID), a traditional herbal formula, has shown the potential to alleviate PD symptoms, but its exact mechanisms remain unclear.
METHODS: We tested PNID in a mouse model of PD induced by a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Mice received different PNID doses to evaluate symptom alleviation. We used behavioral tests and laboratory analyses to study brain changes, including neuron damage assessment, dopamine and tyrosine hydroxylase (TH) measurements, blood-brain barrier (BBB) integrity and microglia evaluation, and inflammatory marker analysis.
RESULTS: PNID treatment alleviated PD symptoms in a dose-dependent manner. High-dose PNID performed similarly to Madopar. Neuron protection: increased dopamine and TH expression. BBB repair: less leakage and fibrinogen accumulation. Regulation of polarization: shifted microglia from M1 to M2 states. Inflammation control: lowered pro-inflammatory factors (IL-6, IL-1β, and TNF-α) while increasing anti-inflammatory factors (IFN-β, IL-10, and IL-4).
CONCLUSIONS: PNID may serve as a promising complementary therapy for PD. Benefits may come from the repair of the BBB, reduction of fibrinogen deposition, and decline in neuroinflammation by modulating microglial polarization.
METHODS: We tested PNID in a mouse model of PD induced by a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Mice received different PNID doses to evaluate symptom alleviation. We used behavioral tests and laboratory analyses to study brain changes, including neuron damage assessment, dopamine and tyrosine hydroxylase (TH) measurements, blood-brain barrier (BBB) integrity and microglia evaluation, and inflammatory marker analysis.
RESULTS: PNID treatment alleviated PD symptoms in a dose-dependent manner. High-dose PNID performed similarly to Madopar. Neuron protection: increased dopamine and TH expression. BBB repair: less leakage and fibrinogen accumulation. Regulation of polarization: shifted microglia from M1 to M2 states. Inflammation control: lowered pro-inflammatory factors (IL-6, IL-1β, and TNF-α) while increasing anti-inflammatory factors (IFN-β, IL-10, and IL-4).
CONCLUSIONS: PNID may serve as a promising complementary therapy for PD. Benefits may come from the repair of the BBB, reduction of fibrinogen deposition, and decline in neuroinflammation by modulating microglial polarization.