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-氨基丁酸能神經功能。γ-氨基丁酸能神經功能的增強可抑制興奮性神經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.