{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T01:55:00Z","timestamp":1791165300801,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2012,5,8]],"date-time":"2012-05-08T00:00:00Z","timestamp":1336435200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:sec><jats:title>BACKGROUND AND PURPOSE<\/jats:title><jats:p>Ca<jats:sub>v<\/jats:sub>3.2 T\u2010type calcium channels, targeted by H<jats:sub>2<\/jats:sub>S, are involved in neuropathic hyperalgesia in rats and ascorbic acid inhibits Ca<jats:sub>v<\/jats:sub>3.2 channels. Therefore, we evaluated the effects of intraplantar (i.pl.) administration of ascorbic acid or topical application of disodium isostearyl 2\u2010O\u2010L\u2010ascorbyl phosphate (DI\u2010VCP), a skin\u2010permeable ascorbate derivative on hyperalgesia induced by NaHS, an H<jats:sub>2<\/jats:sub>S donor, and on neuropathic hyperalgesia.<\/jats:p><\/jats:sec><jats:sec><jats:title>EXPERIMENTAL APPROACH<\/jats:title><jats:p>In rats mechanical hyperalgesia was evoked by i.pl. NaHS, and neuropathic hyperalgesia was induced by L5 spinal nerve cutting (L5SNC) or by repeated administration of paclitaxel, an anti\u2010cancer drug. Dermal ascorbic acid levels were determined colorimetrically.<\/jats:p><\/jats:sec><jats:sec><jats:title>KEY RESULTS<\/jats:title><jats:p>The NaHS\u2010evoked Ca<jats:sub>v<\/jats:sub>3.2 channel\u2010dependent hyperalgesia was inhibited by co\u2010administered ascorbic acid. Topical application of DI\u2010VCP, but not ascorbic acid, prevented the NaHS\u2010evoked hyperalgesia, and also increased dermal ascorbic acid levels. Neuropathic hyperalgesia induced by L5SNC or paclitaxel was reversed by i.pl. NNC 55\u20130396, a selective T\u2010type calcium channel blocker, ascorbic acid or DI\u2010VCP, and by topical DI\u2010VCP, but not by topical ascorbic acid. The effects of i.pl. ascorbic acid and topical DI\u2010VCP in the paclitaxel\u2010treated rats were characterized by the faster onset and greater magnitude, compared with their effects in the L5SNC rats. Dermal ascorbic acid levels in the hindpaw significantly decreased after paclitaxel treatment, but not L5SNC, which was reversed by topical DI\u2010VCP.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS AND IMPLICATIONS<\/jats:title><jats:p>Ascorbic acid, known to inhibit Ca<jats:sub>v<\/jats:sub>3.2 channels, suppressed neuropathic hyperalgesia. DI\u2010VCP ointment for topical application may be of benefit in the treatment of neuropathic pain.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1476-5381.2012.01835.x","type":"journal-article","created":{"date-parts":[[2012,1,9]],"date-time":"2012-01-09T19:30:06Z","timestamp":1326137406000},"page":"1058-1068","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Topical application of disodium isostearyl 2\u2010O\u2010L\u2010ascorbyl phosphate, an amphiphilic ascorbic acid derivative, reduces neuropathic hyperalgesia in 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