氧化苦參堿具有鎮(zhèn)靜、催眠、降體溫、抗癲癇、改善認知功能、保護腦神經(jīng)和外周神經(jīng)作用。其作用機制可能是激活大麻素2型受體和上調(diào)電壓門控鈣離子N型通道表達，促進抑制性神經(jīng)遞質(zhì)（γ-氨基丁酸、甘氨酸）合成與釋放，下調(diào)γ-氨基丁酸轉(zhuǎn)運體-1表達，使突觸間隙γ-氨基丁酸濃度升高以及上調(diào)γ-氨基丁酸_-A受體表達，從而增強γ-氨基丁酸能神經(jīng)功能。γ-氨基丁酸能神經(jīng)功能的增強可抑制興奮性神經(jīng)遞質(zhì)谷氨酸過度表達并下調(diào)N-甲基-D-天冬氨酸（NMDA）受體和蛋白激酶Cγ表達，從而下調(diào)電壓門控鈣離子L型通道的表達，抑制鈣離子內(nèi)流，阻滯鈣/鈣調(diào)素依賴性蛋白激酶Ⅱ/c-AMP反應(yīng)元件結(jié)合蛋白通路，抑制炎癥反應(yīng)，產(chǎn)生中樞抑制和神經(jīng)保護作用。

Oxymatrine has the effects of sedation, hypnotism, hypothermia, anti-epilepsy, enhancing cognitive function and neuroprotective effect to peripheral nerve, and cranial nerves injury. The active mechanism of oxymatrine may can activate cannabine receptor-2 and up-regulate the expression of N-type voltage-gated calcium channels, improve synthesis and release of inhibitory neurotransmitters, γ-aminobutyric acid (GABA) and glycine, down-regulate the expression of GABA transporter 1 (GAT- 1), increase the concentration of GABA in synaptic cleft, and up-regulate the expression of GABAA receptor, thus strengthen GABAergic nerve function. Enhancement of GABAergic nerve function can inhibit the expression of excitatory neurotransmitter, glutamic acid, N-methyl-D-aspartate (NMDA) receptor, and protein kinase Cγ, thus down-regulate the expression of L-type voltagegated calcium channels, and inhibit Ca²⁺ influent, and blocking CaMKⅡ/CREB pathway to inhibit inflammation and product central suppression and neuroprotection.