Marcus Vinicius Gomez
Background: The molecular mechanisms underlying the chronic pain associated with pancreatitis are poorly understood. Hypercalcemia is a risk factor
and the role of cytosolic calcium is described as a modulator of pancreatitis. Blockade of Ca2+ signals may be useful as prophylactic treatment of
pancreatitis. Agents that modulate the activity of the Voltage-Sensitive Calcium Channels (VSCCs) exhibit experimentally and clinically significant pain
relief in visceral pain. Between these agents, the toxins Phα1β and ω-conotoxin MVIIA are effectively reducing the chronic pain in rodent models.
Patients and Methods: AP was induced in rats that received 5 times hourly an intraperitoneal injection of cerulein (5 μg/kg in 100 μL of volume).
Blood serum pancreatic enzymes and ROS analysis were monitored after 8 hours of the first injection cerulein. Behavioral testing of the nociceptive
state of the abdominal area was included in the study. Results: Compared with control groups, rats receiving cerulein demonstrated an increase
in withdrawal events after analgesimeter stimulation. The abdominal mechanical hyperalgesia was reduced after application of the VSCCs
blockers ω-conotoxin MVIIA, Phαβ native and recombinant CTK-01512-2. The treatments reduced the cerulein-induced increase in ROS,
amylase and lipase levels. Phα1β and CTK 01512-2 did not affect the horizontal and vertical exploration activities while ω-conotoxin MVIIA
increased then. Conclusion: These results indicate that animals injected with cerulein-induced experimental pancreatitis expressed by visceral
hyperalgesia, ROS, serum amylase and lipase characteristics of pancreatitis. The treatments of the animals with the VSCCs reduced the effects of
pancreatitis.
Published Date: 2024-05-09; Received Date: 2024-02-12
