苦參堿類生物堿（包括有苦參堿、氧化苦參堿、氧化槐定堿、槐果堿、氧化槐果堿等）具有鎮(zhèn)痛作用，鎮(zhèn)痛特征是以中樞性為主、無成癮性和耐藥性，綜述其鎮(zhèn)痛作用及作用機制研究進展?？鄥A類生物堿的中樞性鎮(zhèn)痛作用機制可能是：激活大麻素受體-2和上調電壓門控鈣離子N-型通道表達，促進抑制性神經(jīng)遞質（γ-氨基丁酸、甘氨酸）合成和釋放，下調GAT-1表達，使突觸間隙γ-氨基丁酸濃度升高以及上調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)遞質谷氨酸過度表達并下調NMDA受體和蛋白激酶Cγ表達，降低NMDA受體對谷氨酸的興奮性，從而下調電壓門控鈣離子L-型通道的表達，抑制鈣離子內流，阻滯CaMKⅡ/CREB通路，減輕炎癥反應和產(chǎn)生鎮(zhèn)痛作用。

Matrine-type alkaloids including matrine, oxymatrine, oxysophoridine, sophocarpine, and oxysophocarpine, which have antinociceptive effects with the characteristics of central, no addiction, and no drug-tolerance. This review summarizes the research progress of antinociceptive effects and related mechanisms of matrine-type alkaloids. Central antinociceptive mechanism of matrine-type alkaloids may be to activate cannabine receptor-2, up-regulate the expression of N-type voltage-gated calcium channels, improve the 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 GABA receptor, thus strengthening GABAergic nerve function. Enhancement of GABAergic nerve function can inhibit the over expression of excitatory neurotransmitter glutamic acid, and down-regulate the expression of N-methyl-D-aspartate (NMDA) receptor, and protein kinase Cγ to decrease the excitation of NMDA receptor response to glutamate, thus down-regulating the expression of L-type voltage-gated calcium channels, inhibiting Ca²⁺ influent, and blocking CaMKⅡ/CREB pathway to inhibit inflammation and produce analgesic action.