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 model | Inhibitor of enzymes that degrade endocannabinoids | Effects | Effects of CB receptor antagonists on the activity of the compound | Reference | Chemotherapy drug | Animal |
| Vincristine | Male SD rats | FAAH inhibitor ST4070 | Suppressed established mechanical allodynia | No antagonists were used against vincristine | [28] | Cisplatin | Male C3H/HeN mice | FAAH inhibitor URB597 | Delayed the onset and decreased the magnitude of mechanical and heat hyperalgesia | CB1 antagonist AM281 antagonised | [25] | Suppressed established mechanical and thermal hyperalgesia | CB2 antagonist AM630 had no effect | Cisplatin | Male SD rats | FAAH inhibitors URB597 and URB937 | Suppressed established mechanical and cold allodynia | CB1 antagonist AM251 antagonised | [24] | MGL inhibitor JZL184 | CB2 antagonist AM630 had no effect | Cisplatin | Male C3H/HeN mice | MGL inhibitor JZL184 | Prevented the development of mechanical hyperalgesia | CB1 receptor antagonist AM281 antagonised | [26] | Suppressed established mechanical allodynia | CB2 receptor antagonist AM630 had no effect | Paclitaxel | Male CD1 and C57BL/6J mice | URB597 and JZL184 | Suppressed mechanical and cold allodynia | Antagonists were not tested | [29] |
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FAAH, fatty acid amide hydrolase; MGL, monoacylglycerol lipase; SD, Sprague-Dawley.
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