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Article Publish Status: FREE
Abstract Title:

Berberine Ameliorates Brain Inflammation in Poloxamer 407-Induced Hyperlipidemic Rats.

Abstract Source:

Int Neurourol J. 2019 Nov ;23(Suppl 2):S102-110. Epub 2019 Nov 30. PMID: 31795609

Abstract Author(s):

Mia Kim, Tae-Woon Kim, Chang-Ju Kim, Mal-Soon Shin, Minha Hong, Hye-Sang Park, Sang-Seo Park

Article Affiliation:

Mia Kim

Abstract:

PURPOSE: Hyperlipidemia, which promotes the development of atherosclerosis, ischemic stroke, and other forms of brain injury, can be induced by poloxamer-407. Berberine is a primary pharmacological active component of Coptidis Rhizoma that has a number of therapeutic activities. This study investigated the effects of berberine on poloxamer-407-induced brain inflammation by evaluating its effects on short-term memory, cell proliferation, inflammation, and apoptosis in the hippocampus.

METHODS: To induce hyperlipidemia in a rat model, 500 mg/kg of poloxamer-407 was injected intraperitoneally. Berberine was orally administered to the rats in the berberine-treated groups once a day for 4 weeks. The step-down task avoidance task was performed to measure short-term memory. An analysis of serum lipids, immunohistochemistry for 5-bromo-2'-deoxyuridine, glial fibrillary acidic protein (GFAP), and ionized calcium-binding adapter molecule 1 (Iba1) in the dentate gyrus, and western blot analysis for Bax, Bcl-2, and cytochrome c in the hippocampus were performed.

RESULTS: In hyperlipidemic rats, berberine reduced the levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol and increased the level of high-density lipoprotein cholesterol in hyperlipidemic rats. Berberine also increased cell proliferation and short-term memory, as well as decreasing the expression of GFAP, Iba1, Bax, and cytochrome c and increasing Bcl-2 expression.

CONCLUSION: Berberine treatment improved short-term memory in hyperlipidemia by increasing neuronal proliferation and inhibiting neuronal apoptosis. Berberine treatment also improved lipid metabolism.

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