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Figure 3 | Molecular Pain

Figure 3

From: Impact of central and peripheral TRPV1 and ROS levels on proinflammatory mediators and nociceptive behavior

Figure 3

ROS Generation. A - Lumbar Spinal Cord after K/C Induced Knee Joint Inflammation. Cumulative generation of ROS is detected by conversion of the fluorescent indicator DHE in the dorsal horn of the L4 spinal cord segment in rats with k/c induced knee joint arthritis (6 h) (n = 4). B - ROS Generation Is Blocked by ROS Scavenger PBN. Much less DHE is observed in spinal cords of rats pretreated i.p. with ROS scavenger, PBN, 1 h prior to induction of knee joint inflammation with k/c (n = 4). Tissues were collected from paraformaldehyde perfused rats 6 h after induction of k/c knee joint arthritis. C - TRPV1 Agonist Induces ROS in Human SW982 Synoviocytes. Enhanced hydroxyl radical (HO•) production is induced by treatment of cultured clonal human SW982 synoviocytes with TRPV1 agonist resiniferatoxin. SW982 cells were incubated in bath saline (37°C) containing 2.5 mM salicylic acid and 100 nM resiniferatoxin (res) (n = 4) or vehicle (cont) (n = 4). After a 6 h incubation samples of extracellular solution were analyzed for stable ROS metabolites, 2,3- and 2,5-dihydroxybenzoic acid (2,3-DHBA and 2,5-DHBA), by HPLC with electrochemical detection as pictogram per microliter (pg/μl).*- indicates statistically significant difference (p < 0.05) between control and resiniferatoxin treated cells.

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