Pain Research and Management / 2018 / Article / Tab 2

Review Article

Targeting the Endocannabinoid System for Prevention or Treatment of Chemotherapy-Induced Neuropathic Pain: Studies in Animal Models

Table 2

Effects of inhibitors of enzymes that degrade endocannabinoids in animal models of CINP.

CINP modelInhibitor of enzymes that degrade endocannabinoidsEffectsEffects of CB receptor antagonists on the activity of the compoundReference
Chemotherapy drugAnimal

VincristineMale SD ratsFAAH inhibitor ST4070Suppressed established mechanical allodyniaNo antagonists were used against vincristine[28]
CisplatinMale C3H/HeN miceFAAH inhibitor URB597Delayed the onset and decreased the magnitude of mechanical and heat hyperalgesiaCB1 antagonist AM281 antagonised[25]
Suppressed established mechanical and thermal hyperalgesiaCB2 antagonist AM630 had no effect
CisplatinMale SD ratsFAAH inhibitors URB597 and URB937Suppressed established mechanical and cold allodyniaCB1 antagonist AM251 antagonised[24]
MGL inhibitor JZL184CB2 antagonist AM630 had no effect
CisplatinMale C3H/HeN miceMGL inhibitor JZL184Prevented the development of mechanical hyperalgesiaCB1 receptor antagonist AM281 antagonised[26]
Suppressed established mechanical allodyniaCB2 receptor antagonist AM630 had no effect
PaclitaxelMale CD1 and C57BL/6J miceURB597 and JZL184Suppressed mechanical and cold allodyniaAntagonists were not tested[29]

FAAH, fatty acid amide hydrolase; MGL, monoacylglycerol lipase; SD, Sprague-Dawley.

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