Calcium channels blockers toxins attenuate abdominal hyperalgesia and inflammatory response associated with the cerulein-induced acute pancreatitis in rats

The Antihyperalgesic Effects of the Calcium Channel Blocker CTK 01512-2 Toxin in Persistent Pain Models

“…Phα1β pointed out as a promising alternative for treating bladder dysfunctions [20] and for reverting glial plasticity upon peripheral in ammation [23]. It was shown recently that calcium channels blockers' toxins attenuated abdominal hyperalgesia and in ammatory response associated with the cerulein-induced acute pancreatitis in rats [22]. The recombinant peptide also showed analgesic effects in orofacial pain models [21] and neuroprotective effects against neurotoxicity induced by 3-nitropropionic acid in rats [26].…”

“…1. The protocols of treatment for all the tested drugs (doses, route of administration, and time of injection) were chosen following previous publications [43,44,12,38,22,37] 2.8. Behavioral tests…”

“…To block the VGCCs, the channelactivating current must be disrupted, whereby the blockers and the toxins normally act by modulating the G-protein-coupled receptors [18,19,17]. CTK 01512-2 toxin has proved to have a therapeutically potential in preclinical studies of pain models, such as in ammatory [20][21][22][23][24], neuropathic [13,25,24], energy metabolism and cell death [26], cancer [27][28][29], multiple sclerosis [12], and bromyalgia [30,31]. Based on previous ndings, herein, we have investigated whether CTK 01512-2 central and systemic treatments can produce analgesic and anti-in ammatory effects in both CPIP and neuropathy induced by paclitaxel models in order to provide further evidence on its related pain mechanisms.…”

Analgesic effects of Phα1β toxin: a review of mechanisms of action involving pain pathways

“…administration blocking NVACC [131], anti-hyperalgesic effects on cancer melanoma cells [36], and inhibition of capsaicin nociceptive behaviour [37]. Intrathecal treatment with recombinant peptides also modulates other events such as neuroinflammation and neurodegeneration [132,133]. In addition to pain signalling, there is evidence that VACC also participate in the development of some CNS disorders.…”

“…In rodents, i.p. injections of cerulein induces AP as evidenced by an increase in hyperalgesic pain, inflammatory infiltration, amylase and lipase secretion, and reactive oxygen species formation [133]. Phα1β and its recombinant CTK 01512-2 form, both blockers of the TRPA1 receptor [12] and HVACC [10], abolished these effects [133] after i.t.…”