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Figure 3 | Molecular Pain

Figure 3

From: An LPA species (18:1 LPA) plays key roles in the self-amplification of spinal LPA production in the peripheral neuropathic pain model

Figure 3

Blockade of nerve injury-induced cPLA 2 and iPLA 2 activations. (a and b) Activation of spinal cPLA2 (panel a ) and iPLA2 (panel b ) were detected by cPLA2 and iPLA2 activity assays at defined time points after nerve injury. The capital letter “C” represents the control group (naive mice). (c and d) After pre-treatments of vehicle, MK-801, CP-99994, AACOCF3, BEL (each 10 nmol, i.t.) and minocycline (30 mg/ml, i.p.) before nerve injury, the activities of spinal cPLA2 (panel c ) and iPLA2 (panel d ) at 1 h after injury were evaluated. The “veh”, “MK”, “CP”, “AA” and “mino” represent vehicle, MK-801, CP-99994, AACOCF3 and minocycline, respectively. (e and f) Activities of cPLA2(panel e ) and iPLA2 (panel f ) were measured at 1 h after injury using the Lpar1- and Lpar3-deficient mice. “WT” represents the wide-type mice. (g) PLA1 activity in the spinal dorsal horn was measured by PLA1 activity assay at time-course points after nerve injury. Data represent means ± SEM from experiments using 3-6 mice. *p < 0.05, versus with the control group; #p < 0.05, versus with the vehicle/WT-injury group.

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Molecular Pain

ISSN: 1744-8069

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