纳洛肼及14-羟基双氢吗啡肼与阿片受点结合的可逆性

用纳洛肼(NZI,1×10^-5M)或14-羟基双氢吗啡肼(HZI,1×10^-6)与大鼠脑匀浆P₂膜制备保温后,以Tris缓冲液反复洗涤,阿片受点可完全恢复与[³H]双氢吗啡([³H]DHM)的结合能力。在离体豚鼠回肠纵肌(GPI)试验中,HZI对电刺激收缩的抑制及NZI对吗啡(Mor)抑制作用的对抗亦皆可被洗掉,此外HZI对收缩的抑制还可被纳洛酮(Nal)所逆转,说明它们与阿片受点的结合都是可逆的。HZI镇痛作用ED₅₀为1.3 mg/kg(小鼠热板法SC),略强于Mor(3 mg/kg),持续时间与Mor相似。NZI对Mor镇痛的对抗可持续十余小时。     

利血平与优降宁对动物痛阈和吗啡镇痛作用影响因素探讨

采用三种测痛方法,观察了利血平、优降宁对小鼠、大鼠正常痛阈和吗啡镇痛作用的影响,结果表明:ip利血平2 mg/kg,优降宁100 mg/kg均能明显抑制小鼠扭体反应;ip利血平1 mg/kg能明显提高小鼠热板反应时间,但ip优降宁75 mg/kg无明显影响;ip利血平6 mg/kg,优降宁75 mg/kg对大鼠甩尾反应时间均无明显影响;利血平(小鼠0.5～1.0 mg/kg,大鼠2 mg/kg ip)能明显对抗吗啡镇痛作用;优降宁(小鼠35 mg/kg,大鼠50 mg/kg ip)能明显增强吗啡镇痛作用,并能“逆转”利血平对抗吗啡镇痛作用。其“逆转”作用的强弱取决于利血平、优降宁给药的先后次序。     

利血平与优降宁对动物痛阈和吗啡镇痛作用影响因素探讨

采用三种测痛方法,观察了利血平、优降宁对小鼠、大鼠正常痛阈和吗啡镇痛作用的影响,结果表明:ip利血平2 mg/kg,优降宁100 mg/kg均能明显抑制小鼠扭体反应;ip利血平1 mg/kg能明显提高小鼠热板反应时间,但ip优降宁75 mg/kg无明显影响;ip利血平6 mg/kg,优降宁75 mg/kg对大鼠甩尾反应时间均无明显影响;利血平(小鼠0.5～1.0 mg/kg,大鼠2 mg/kg ip)能明显对抗吗啡镇痛作用;优降宁(小鼠35 mg/kg,大鼠50 mg/kg ip)能明显增强吗啡镇痛作用,并能“逆转”利血平对抗吗啡镇痛作用。其“逆转”作用的强弱取决于利血平、优降宁给药的先后次序。     

东莨菪碱对痛和镇痛的影响

对家兔作钾离子透入法测痛,腹腔注射东莨菪碱4mg/kg,给药后30分钟痛阈提高49%。静脉注射同样剂量的东莨菪碱,给药后20分钟痛阈提高37%。侧脑室注射5 μg/只后20分钟痛阈提高53%。这些结果表明东莨菪碱有一定强度的镇痛作用。与度冷丁(60 mg/kg腹腔注射)合用痛阈提高147%,而单用度冷丁病阈升高93%,提示两药合用有协同作用。对小白鼠用热板法测痛,腹腔注射东莨菪碱1.25 mg/kg,给药后15分钟病阈提高62%。与小剂量度冷丁(10 mg/kg腹腔注射)合用,给药后15分钟痛阈提高126%,而单用小剂量度冷丁痛阈仅提高23%。这些与用家兔实验的结果一致。给家兔侧脑室注射去甲肾上腺素20 μg/只后,10分钟时痛阈下降46%,并能减弱度冷丁的镇痛作用。东莨菪碱与去甲肾上腺素合用,则能拮抗后者的抗镇痛作用。因此推测东莨菪碱的镇痛和加强度冷丁镇痛的作用,可能与其抗去甲肾上腺素的作用有关。     

碘化二甲基木防己碱对实验性心律失常及心肌电活动的作用

静脉注射碘化二甲基木防己碱(DMT)1mg/kg,有对抗乌头碱诱发大鼠心律失常的作用。腹腔注射DMT0.25mg/kg,有对抗氯仿-肾上腺素诱发家兔心律失常的作用。腹腔注射DMT1.5mg/kg,对抗哇巴因诱发豚鼠心律失常,使豚鼠心室肌细胞动作电位平台期延长。DMT3.0×10^-6使家兔离体心房肌功能不应期延长。     

不同药物对眼镜蛇神经毒素镇痛效应的影响

用电尾嘶叫法测量大鼠病阈。给大鼠侧脑室注射相当于1/10im有效量的眼镜蛇神经毒素(NT)可明显提高大鼠痛阈。利血平5mg/kg,ip并不影响NT的镇痛作用。纳洛酮3mg/kg,ip仅能轻度降低NT的镇痛作用。阿托品1mg/kg,im却能完全拮抗NT的镇痛效应。在对吗啡急性耐受的大鼠上,NT仍能产生明显的镇痛效应。结果提示,NT的镇痛部位可能位于中枢神经系统内。其镇痛机理可能涉及中枢的乙酰胆碱能系统。     

醋酸棉酚和15甲基PGF2α甲酯对大鼠子宫胞浆雌激素受体的影响

假孕大鼠口服醋酸棉酚40和80 mg/kg连续5天,平均每个子宫的胞浆蛋白和雌激素受体量明显减少。以每mg蛋白计,雌激素受体浓度同对照组差异不显著。幼大鼠口服醋酸棉酚40mg/kg连续8天,作饱和分析测得对照组和给药组K_d值分别为1.04×10^-10和1.09×10^-10mol。最大受体结合数分别为432.0和358.8 fmol/子宫。实验发现棉酚在高浓度时对³H-雌二醇同其受体的结合有抑制作用。15甲基PGF_2α甲酯对假孕大鼠子宫胞浆蛋白水平和雌激素受体均无明显影响。     

尼索地平对大鼠离体肺动脉和肺动脉高压的影响

目的 观察尼索地平(nifedipine,NIS)对KCl和去氧肾上腺素(phenylephrine,PHE)所致离体大鼠肺动脉收缩的作用,同时研究其对野百合碱诱导的肺动脉高压(pulmonary hypertention,PH)大鼠的影响。方法 ①采用离体血管实验法,以KCl和PHE在含钙离子和不含钙离子的K-H液中预收缩离体大鼠肺动脉环,观察NIS对血管收缩的影响。②取40只Wistar大鼠随机分为正常组、模型组、NIS组和硝苯地平(NIF)组,每组10只,采用野百合碱(50 mg·kg^-1)皮下注射建立大鼠PH模型,连续灌胃给药21 d。采用右心导管法测定mPAP、mRVP、maxPAP和maxRVP,并计算各组大鼠的RVHI和LI。结果 ①在含钙离子的K-H液中,NIS抑制KCl(20,40,60 mmol·L^-1)和PHE(1×10^-7,5×10^-7,1×10^-6 mol·L^-1)所致血管收缩的IC₅₀分别为0.87×10^-8,1.41×10^-8,8.32×10^-8 mol·L^-1和0.56×10^-7,4.27×10^-7,1.28×10^-6 mol·L^-1。在无钙离子K-H液中,NIS无抑制离体血管收缩的作用。②模型组大鼠mPAP、mRVP、maxPAP、maxRVP、RVHI和LI均显著高于正常组(P<0.01),NIS组和NIF组大鼠的上述指标均显著低于模型组(P<0.05)。结论 NIS有抑制大鼠肺动脉收缩的作用,对野百合碱诱导的大鼠PH有治疗作用。     

眼镜蛇神经毒素的镇痛作用

眼镜蛇神经毒素(NT)在小鼠热板及大鼠电尾嘶叫测痛模型,都显示出明显的镇痛作用,并有剂量-效应关系。注射NT 0.022mg/kg,2h后,大鼠痛阈出现显著上升,3h后达到较佳效果,并能保持其效应强度达24h。连续给小鼠注射NT 0.023mg/kg,持续9d,小鼠并不产生耐受现象。结果提示,NT的镇痛机理可能与吗啡不同。     

7-甲氧基-4′-羟基-3′-二乙胺甲基异黄酮(MHDF)对大鼠血流动力学和主动脉的作用

本实验观察了MHDF对整体大鼠血流动力学和离体大鼠胸主动脉的作用。结果表明iv MHDF(3～12.8 mg/kg)能降低大鼠左心室±dp/dt_max,V_max,V_pm和LVSP,延长T-dp/dt_max,减慢心率。MHDF还能舒张大鼠胸主动脉,ED₅₀为6.5×10^-6mol/L;非竞争拮抗NA和CaCl₂致主脉收缩,pD₂′为3.11±0.21和3.73±0.07;抑制高K⁺致主动脉收缩,IC₅₀为1.76×10^-5mol/L。提示MHDF对血管的作用与α受体阻断剂不同,而可能与钙拮抗有关。     

Analysis of the mechanisms underlying the antinociceptive effect of the extracts of plants from the genus Phyllanthus

• 1.1. We examine some of the mechanisms underlying the analgesic effects of the hydroalcoholic extracts (HE) of Phyllanthus urinaria and P. niruri against formalin-induced nociception in mice. In addition, we also investigate the action of both HEs against capsaicin-mediated pain.
• 2.2. Both prazosin and yohimbine (0.15 mg/kg, i.p.) induced a marked inhibition of the analgesic effect caused by phenylephrine (10 mg/kg, i.p.) and clonidine (0.1 mg/kg, i.p.), respectively, but had no effect on the antinociceptive action caused by HE of P. urinaria (10 mg/kg, i.p.) or P. niruri (30 mg/kg, i.p.).
• 3.3. N^G-nitro-l-arginine (l-NOARG, 75 mg/kg, i.p.) caused marked analgesic effect against the second phase of formalin-induced pain. Treatment of animals with l-arginine (600 mg/kg) completely antagonized the antinociceptive effect of l-NOARG but had no significant effect against the HE of P. urinaria (10 mg/kg, i.p.) or P. niruri (30 mg/kg, i.p.) analgesic properties.
• 4.4. The antinociceptive effects caused by the HEs of P. urinaria (10 mg/kg, i.p.) and P. niruri (30 mg/kg, i.p.) were unaffected by methysergide (5 mg/kg, i.p.), p-chloro-phenylalanine-methyl-ester (100 mg/kg, i.p., once a day for 4 consecutive days) or after previous adrenalectomy of animals.
• 5.5. The HE of P. urinaria and P. niruri given either intraperitoneally (1–30 mg/kg) or orally (25–200 mg/kg) caused marked and dose-related inhibition of capsaicin-induced pain with ID₅₀ of 2.1 and 6.1 mg/kg given intraperitoneally and 39 and 35 mg/kg given orally, respectively.

     

Comparative study of the anti-inflammatory and antinociceptive effects of two varieties of Punica granatum

Context: Studies have shown that pomegranate, Punica granatum Linn. (Lythraceae), has remarkable biological and medicinal properties.

Objective: This work aimed to explore and compare the analgesic and anti-inflammatory activities of the methanol extract (MoE) obtained from fruit peels of two varieties of pomegranate: Amrouz (MoEA) and Sefri (MoES).

Materials and methods: Antinociceptive activity of MoEA and MoES was examined using four models of pain. The extracts were administered by the intraperitoneal route (i.p.) in writhing (50, 100 and 150?mg/kg) and formalin tests (25, 50 and 100?mg/kg) and by intra-cerebroventricular injection (i.c.v.) in hotplate and tail-immersion tests (10, 25 and 50 µg/3 µl/rat). anti-inflammatory activity was studied using the hind paw egg albumin test (50, 100 and 150?mg/kg, i.p.).

Results: In the writhing test, the index of pain inhibition (IPI) was 52% for MoEA (150?mg/kg, i.p.) and 29% for MoES (150?mg/kg, i.p.). In the formalin test, the IPI of early and late phase were, respectively, 75% and 82% for MoEA (100?mg/kg, i.p.) and 8% and 63% for MoES (100?mg/kg, i.p.). In the hotplate and tail-immersion test, MoEA and MoES increased in a dosedependent manner the reaction latency to the thermal stimuli. MoEA seems to be more potent than MoES. Only the analgesic effect of MoEA was partially inhibited by pretreatment with naloxone. Both extracts exerted a significant anti-inflammatory effect.

Discussion and conclusions: The results demonstrated that P. granatum contains active constituents, which possess antinociceptive and anti-inflammatory activity, justifying its popular uses.     

Dopaminergic Involvement in Improving Effects of Dynorphin A-(1-13) on Galanin-Induced Impairment of Passive Avoidance Learning in Mice

The present study was designed to clarify whether dopaminergic systems are involved in the effects of dynorphin A-(1-13), an endogenous κ-opioid receptor agonist, on the galanin-induced impairment of passive avoidance learning in mice. Galanin (0·3 μg, i.c.v.) shortened step-down latency of passive avoidance learning, while the dopamine D₁ receptor agonist SKF 38393 (3 and 10 mg/kg, s.c.), the dopamine D₂ receptor agonist RU 24213 (0·3 and 1 mg/kg, s.c.), the dopamine D₁ receptor antagonist SCH 23390 (0·01 and 0·03 mg/kg, i.p.) or the dopamine D₂ receptor antagonist S(−)-sulpiride (10 and 30 mg/kg, i.p.) failed to influence it. Dynorphin A-(1-13) (3 μg, i.c.v.) and SKF 38393 (10 mg/kg, s.c.) markedly improved the galanin (0·3 μg, i.c.v.)-induced shortening of step-down latency. However, RU 24213 (0·3 and 1 mg/kg, s.c.), SCH 23390 (0·01 and 0·03 mg/kg, i.p.) or S(−)-sulpiride (10 and 30 mg/kg, i.p.) did not affect the galanin (0·3 μg, i.c.v.)-induced shortening of step-down latency. In contrast, SCH 23390 (0·3 mg/kg, i.p.) significantly reversed the improving effects of dynorphin A-(1-13) (3 μg, i.c.v.) on the galanin (0·3 μg, i.c.v.)-induced dysfunction of passive avoidance learning, although SKF 38393 (1 and 3 mg/kg, s.c.), RU 24213 (0·3 and 1 mg/kg, s.c.) or S(−)-sulpiride (10 and 30 mg/kg, i.p.) did not influence the effects of dynorphin A-(1-13) (3 μg, i.c.v.). These results suggest that dynorphin A-(1-13) improves the galanin-induced amnesia resulting from indirect stimulation of dopamine D₁ receptors. © 1997 John Wiley & Sons, Ltd.     

Analgesic Activity of Cistus laurifolius in Mice

The possible analgesic activity of Cistus laurifolius extracts has been evaluated by using tail flick and acetic acid-induced writhing tests in mice. The chloroform extract (500?mg/kg, i.p.) and the precipitated fraction (10, 30, 100?mg/kg, i.p.) obtained from C. laurifolius leaves showed significant analgesic activity on tail flick assay, while aqueous, ethanol and butanol extracts of the plant had no activity on the same test. Chloroform extract (500?mg/kg, i.p.) and precipitate fraction (30?mg/kg, i.p.) also inhibited number of writhings induced by acetic acid. These observations suggest that C. laurifolius leaves possess antinociceptive compound(s) which act through a central mechanism.     

GABAA-antagonists and baclofen analgesia

1. Intraperitoneal (i.p.) injection of different doses of baclofen (5, 7.5 and 10 mg/kg) induced analgesia in tail-flick test. The effect was dose-dependent. 2. The antinociception induced by baclofen (10 mg/kg, i.p.) was decreased in animals pretreated with bicuculline (1.5 mg/kg, i.p., 30 min), but not with naloxone (1.5 mg/kg, i.p., 30 min). 3. In picrotoxin (1 mg/kg, i.p., 15 min) pretreated mice, baclofen (5 mg/kg, i.p.) showed a significant analgesic effect. 4. Morphine (6 mg/kg, s.c.) induced analgesia which was antagonized by naloxone pretreatment (1.5 mg/kg, i.p.), while bicuculline or picrotoxin did not alter the morphine response. 5. These data suggest that a part of analgesic effect of baclofen may be mediated through GABAA receptor sites, and differs from that of morphine.     

A COMPARISON OF THE MUSCARINIC ANTAGONIST ACTIONS OF PANCURONIUM AND ALCURONIUM

• 1 In the pithed rat, muscarine (2.5–10μg/kg i.v.) normally produced bradycardias, but tachycardias were seen in the presence of pancuronium (0.1–1.0mg/kg i.v.) and alcuronium (0.1–5.0mg/kg i.v.).
• 2 The tachycardia was probably a result of muscarinic receptor stimulation, because it was antagonized by atropine (10μg/kg i.v.) and pirenzepine (10–30μg/kg i.v.). The location of these muscarinic receptors is probably within the sympathetic ganglia since the tachycardias were inhibited by pretreatment with propranolol (1mg/kg i.v.) or reserpine (5mg/kg i.p. 24 h prior to study).
• 3 In the rat isolated atria preparation, pancuronium was 86 times more potent as an antagonist of the effects of muscarine than in the rat isolated superior cervical ganglion. The mechanism of action in both tissues may be non-competitive.
• 4 Pancuronium selectivity antagonized atrial inhibitory muscarinic responses compared to excitatory muscarinic responses in sympathetic ganglia in the rat.

     

Analgesic,anti-inflammatory and anti-platelet activities of the methanolic extract of <Emphasis Type="Italic">Acacia modesta</Emphasis> leaves

The current study was aimed to evaluate Acacia modesta for analgesic, anti-inflammatory, and anti-platelet activities. The analgesic and anti-inflammatory effects were assessed in rodents using acetic acid and formalin-induced nociception, hot plate and carrageenan-induced rat paw oedema tests. The intraperitoneal (i.p.) administration of the methanolic extract (50 and 100 mg/kg) produced significant inhibition (P < 0.01) of the acetic acid-induced writhing in mice and suppressed formalin-induced licking response of animals in both phases of the test. In the hot plate assay the plant extract (100 mg/kg) increased pain threshold of mice. Naloxone (5 mg/kg i.p.) partially reversed the analgesic effect of the extract in formalin and hot plate tests. A. modesta (100 and 200 mg/kg i.p.) exhibited sedative effect in barbiturate-induced hypnosis test similar to that produced by diazepam (10 mg/kg i.p.). The plant extract (50–200 mg/kg i.p.) produced marked anti-inflammatory effect in carrageenan-induced rat paw oedema assay comparable to diclofenac and produced a dose-dependent (0.5–2.5 mg/mL) inhibitory effect against arachidonic acid induced platelet aggregation. These data suggest that A. modesta possesses peripheral analgesic and anti-inflammatory properties, with analgesic effects partially associated with the opioid system.     

Augmentative effect of spinosin on pentobarbital-induced loss of righting reflex in mice associated with presynaptic 5-HT1A receptor

Objectives This study investigated whether spinosin potentiates pentobarbital‐induced loss of righting reflex (LORR) in mice via 5‐HT_1A receptors. Methods Our primary endpoint for sedation was LORR. In addition, the basal rectal temperature was measured. Key findings The results demonstrated that the 5‐HT_1A agonist 8‐OH‐DPAT (s.c.) induced reductions in duration of LORR at 0.1, 0.5 and 1.0 mg/kg (P < 0.01), and prolongation of LORR latency at 0.5 and 1.0 mg/kg (s.c., P < 0.01) in pentobarbital (45 mg/kg, i.p.)‐treated mice. This effect of 8‐OH‐DPAT was antagonized either by 5‐HT_1A antagonist p‐MPPI (5 mg/kg, i.p.) or by spinosin (15 mg/kg, i.g.) with significance, respectively. Co‐administration of spinosin and p‐MPPI both at ineffective doses (spinosin at 5.0 mg/kg, i.g. and p‐MPPI at 1.0 mg/kg, i.p.) showed significant augmentative effects in reducing latency to LORR, and increasing LORR duration (P < 0.01) in pentobarbital‐treated mice. On the other hand, spinosin inhibited 8‐OH‐DPAT‐induced hypothermia, which has been generally attributed to the activation of somatodendritic 5‐HT_1A autoreceptors in mice. Conclusions Based on our previous results and the present data, it should be presumed that presynaptic 5‐HT_1A autoreceptor mechanisms may be involved in the inhibitory effect of spinosin on 8‐OH‐DPAT‐induced hypothermia and also in the potentiating effect of spinosin on pentobarbital‐induced LORR in mice.     

Role of N-methyl-d-aspartic acid and cholecystokinin receptors in apomorphine-induced aggressive behaviour in rats

We studied the aggressive behaviour induced by repeated treatment with apomorphine, a dopamine agonist (0.5 mg/kg s.c. twice daily, 10 days), in rats. The first signs of defensive aggressiveness appeared on the third day of apomorphine treatment and were generally seen on the 7th day. Aggressiveness induced by a challenge dose of apomorphine (0.5 mg/kg s.c.) on the 11th day was antagonized by haloperidol (0.05 and 0.1 mg/kg i.p.) and clozapine (10 mg/kg i.p.). An antagonist of N-methyl-D-aspartate (NMDA)-gated channels, dizocilpine (MK-801), also blocked the aggressive behaviour at 0.25 and 0.5 mg/kg i.p. but caused ataxia. When dizocilpine (0.25 mg/kg i.p.) and apomorphine were coadministered for 10 days, aggressive behaviour did not develop. At 0.025 mg/kg i.p., dizocilpine even accelerated the appearance of apomorphine-induced aggressive behaviour, which manifested on the 3rd day in all rats. In a separate study, a 7-day treatment with dizocilpine (0.25–1 mg/kg i.p.) of rats, sensitized by a prior 10-day apomorphine treatment, did not reverse the established aggressive behaviour. The coadministration of apomorphine and cholecystokinin (CCK)-A or -B antagonists, devazepide or L-365,260 (0.01–2.5 mg/kg i.p.) respectively, neither affected development of apomorphine-induced aggressive behaviour nor intensity of aggressiveness in the sensitized rats.In binding studies neither density nor affinity of striatal dopamine D₂ receptors was changed by acute or chronic apomorphine treatment. The number of [³H]pCCK-8 binding sites in the frontal cortex increased already after a single injection of apomorphine. After 10-day administration of apomorphine, a significant upregulation of [³H]pCCK-8 binding sites occurred in the frontal cortex and striatum, but a downregulation was observed in the hippocampus. A challenge dose of apomorphine (0.5 mg/kg s.c.) on the 11th day of experiment, normalized the upregulated CCK receptors in the frontal cortex and striatum. Acute apomorphine did not change [³H]-MK-801 binding in the rat brain. However, in rats treated for 10 days with apomorphine, the number of NMDA-gated channels in open state was increased in the frontal cortex and hippocampus. In these rats, a challenge dose of apomorphine (0.5 mg/kg s.c.) normalized also the in reased number of [³H]-MK-801 binding sites in the frontal cortex.In conclusion, repeated treatment with apomorphine seems to modify the function of dopamine D₂ receptors without affecting their number or affinity. The increased number of NMDA-gated channels in open state appears to be related to this alteration of dopamine D₂ receptors. The increased density of [³H]pCCK-8 binding sites in the frontal cortex may reflect anxiety and fear due to chronic exposure of rats to apomorphine.     

Analgesic Effects of Callus Culture Extracts from Selected Species of Phyllanthus in Mice

Abstract— The aim of this study was to evaluate the analgesic effect of the methanolic extract from callus culture of Phyllanthus tenellus, P. corcovadensis and P. niruri in several models of pain in mice. The extracts (medium containing 2,4-dichlorophenoxyacetic acid) of P. corcovadensis, P. niruri and P. tenellus (3–90 mg kg^?1, i.p.) caused graded inhibition of abdominal constrictions induced by acetic acid (0·6%), with ID50 (i.e. dose that reduced response of control by 50%) values of about 30, 19 and >30 mg kg^?1, respectively. The extract of callus of Phyllanthus obtained in indole-3-butyric acid and indole-3-acetic acid media (3–90 mg kg^?1, i.p.) caused a similar analgesic effect. In the formalin test, the extract of P. tenellus obtained in indole butyric acid medium (3–100 mg kg^?1, i.p.) inhibited only the second phase of formalin-induced pain with an ID50 value of about 100 mg kg^?1. Both the indole acetic acid and indole butyric acid methanolic extracts of P. tenellus and P. corcovadensis (10–100 mg kg^?1, i.p.) dose-dependently inhibited both phases of formalin-induced pain (ID50 values for the second phase were approx. 100 and 52 mg kg^?1, respectively). However, the extract of callus from Phyllanthus failed to affect formalin-induced paw oedema, as well as the response to radiant heat in the tail-flick test. In addition, the analgesic effect of morphine, but not the analgesic effects caused by Phyllanthus callus extract, was fully antagonized by naloxone. Preliminary phytochemical analysis revealed the presence of several compounds having no apparent relationship with alkaloids or flavonoids but showing the presence of phenols. These results indicate that, similar to previous reported data from the extract of P. corcovadensis, the methanolic extracts of callus culture of P. niruri, P. corcovadensis and P. tenellus exhibit potent analgesic properties against neurogenic and inflammatory pain that seem to be unrelated to the activation of opioid mechanisms.