小檗堿通過多靶點機制改善多種病理因素誘導(dǎo)的認知功能障礙。小檗堿通過抑制膽堿酯酶活性、促進乙酰膽堿（Ach）生物合成和M-膽堿樣作用，改善和提高膽堿能神經(jīng)功能，以及通過抗氧化、抗炎、抑制β淀粉樣蛋白（Aβ）和tau蛋白表達、tau蛋白過度磷酸化和對抗Aβ的神經(jīng)損傷的腦神經(jīng)保護機制，防治各種病理因子誘導(dǎo)的認知功能障礙。在基因突變、腦血管疾病、糖尿病腦病、化學(xué)物質(zhì)及術(shù)后損傷等模型中，小檗堿顯著改善學(xué)習(xí)記憶能力，降低海馬神經(jīng)元凋亡及炎癥因子表達，并通過調(diào)節(jié)糖原合酶激酶-3β（GSK3β）、核因子E相關(guān)因子-2（Nrf2）、磷脂酰肌醇-3-激酶/蛋白激酶B（PI3K/akt）等信號通路發(fā)揮神經(jīng)保護作用。建議臨床醫(yī)生應(yīng)該為小檗堿防治認知功能障礙患者找出適宜的劑量范圍，以利于臨床推廣應(yīng)用。

Berberine ameliorates cognitive dysfunction induced by a variety of pathological factors through multi-target mechanisms. It has been shown to improve and enhance cholinergic neurological function through inhibition of cholinesterase activity, promotion of acetylcholine (Ach) biosynthesis and M-choline-like effects, as well as to prevent and control cognitive dysfunction induced by a wide range of pathological factors through cerebral neuroprotective mechanisms such as antioxidant, anti-inflammatory, inhibition of Aβ and tau protein expression, hyperphosphorylation of tau protein, and counteracting the neurological damage of Aβ. In models of genetic mutation, cerebrovascular disease, diabetic encephalopathy, chemical substances and postoperative injury, berberine significantly improved learning and memory ability, reduced hippocampal neuronal apoptosis and inflammatory factor expression, and exerted neuroprotective effects by regulating GSK3β, Nrf2, PI3K/Akt and other signaling pathways. It is suggested that clinicians should find out the appropriate dosage range for berberine to prevent and treat patients with cognitive dysfunction, so as to facilitate the clinical promotion of its application.

R285.5