Freitas Cristina Setim, Baggio Cristiane Hatsuko, Twardowschy André, dos Santos Ana Cristina, Mayer Bárbara, Luiz Ana Paula, dos Santos Cid Aimbiré Moraes, Marques Maria Consuelo Andrade, dos Santos Adair Roberto Soares
Department of Pharmacology, Sector of Biological Sciences, Federal University of Paraná, Curitiba, PR, Brazil.
J Ethnopharmacol. 2009 Apr 21;122(3):468-72. doi: 10.1016/j.jep.2009.01.033. Epub 2009 Feb 3.
Pfaffia glomerata (Spreng) Pedersen (Amaranthaceae) is a medicinal plant known in Brazil as "Paratudo" and "Brazilian ginseng" and is commonly used as tonic, antidiabetic and to treat gastric disorders.
This study evaluates the possible mechanism by which hydroalcoholic extract (HE) of Pfaffia glomerata exerts its antinociceptive effect.
The HE was evaluated in acetic acid and glutamate models of pain or by biting behavior following intrathecal (i.t.) administration of agonists of excitatory aminoacids (EAA) receptors glutamate and pro-inflammatory cytokines, IL-1beta and TNF-alpha in mice.
Oral administration of HE produced dose-dependent inhibition of acetic acid-induced visceral pain and glutamate-induced pain, with ID(50) of 64.6 (47.7-87.5)mg/kg and ID(50) of 370.8 (253.4-542.7)mg/kg, respectively. The HE (300 mg/kg, p.o.) antinociception, in the acetic acid test, was not affected by i.p. treatment of animals with naloxone. In addition, HE (300 mg/kg, p.o.) inhibited the pain-related behaviors induced by i.t. injection of trans-ACPD and TNF-alpha, but not by NMDA, AMPA, kainate or IL-1beta.
Our results suggest that inhibition of glutamatergic metabotropic receptors and TNF-alpha may account for the antinociceptive action reported for the HE in models of chemical pain used in this study.
团花赛亚麻(Pfaffia glomerata (Spreng) Pedersen,苋科)是一种药用植物,在巴西被称为“万能药”和“巴西人参”,常用于滋补、抗糖尿病以及治疗胃部疾病。
本研究评估团花赛亚麻水醇提取物(HE)发挥其抗伤害感受作用的可能机制。
通过醋酸和谷氨酸疼痛模型,或者在小鼠鞘内注射兴奋性氨基酸(EAA)受体谷氨酸以及促炎细胞因子IL-1β和TNF-α的激动剂后观察咬行为,来评估HE。
口服HE对醋酸诱导的内脏痛和谷氨酸诱导的疼痛产生剂量依赖性抑制,ID50分别为64.6(47.7 - 87.5)mg/kg和370.8(253.4 - 542.7)mg/kg。在醋酸试验中,腹腔注射纳洛酮处理动物后,HE(300 mg/kg,口服)的抗伤害感受作用不受影响。此外HE(300 mg/kg,口服)抑制了鞘内注射反式-ACPD和TNF-α诱导的疼痛相关行为,但对NMDA、AMPA、海人酸或IL-1β诱导的行为无抑制作用。
我们的结果表明,抑制谷氨酸能代谢型受体和TNF-α可能是本研究中所报道的HE在化学性疼痛模型中抗伤害感受作用的原因。