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CNS-Sparing Histamine H Receptor Antagonist as a Candidate to Prevent the Diabetes-Associated Gastrointestinal Symptoms. | LitMetric

AI Article Synopsis

  • The study investigates the effects of PF00868087, a histamine H receptor antagonist, on diabetes-related autonomic neuropathy in the intestines of mice.
  • Male BALB/c mice were induced with diabetes, and those treated with PF00868087 showed a significant reduction in abnormal mucus production in the intestines.
  • The findings suggest that PF00868087 may help alleviate gastrointestinal issues related to diabetes by balancing inhibitory and excitatory nerve components in the gut.

Article Abstract

Among the histamine receptors, growing evidence points to the histamine H receptor as a pharmacological candidate to counteract the autonomic neuropathy associated with diabetes. The study aimed to evaluate the effect of PF00868087 (also known as ZPL-868), a CNS-sparing histamine H receptor antagonist, on the autonomic neuropathy of the intestinal tract associated with diabetes. Diabetes was induced in male BALB/c mice by a single high dose of streptozotocin (150 mg/kg). Colorectal specimens from control and diabetic mice, randomized to vehicle or PF0086087 (10, 30, 100 mg/kg/day by oral gavage for 14 days), were processed for morphological and immunohistochemical analysis. A significant overproduction of mucus in the intestinal mucosa of diabetic mice compared to the controls was observed. PF0086087 at the highest dose prevented mucin overproduction. The immunohistochemistry analysis demonstrated that diabetes causes a decrease in the inhibitory component of enteric motility, measured as the percentage of neuronal nitric oxide synthase-positive neurons ( < 0.05) and a parallel increase in the excitatory component evaluated as substance P-positive fibres ( < 0.01). PF0086087 dose-dependently prevented these pathophysiological events. In conclusion, PF0086087 may be an essential tool in preventing nitrergic dysfunction in the myenteric plexus of the distal colon and diabetes-induced gastrointestinal complications.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8961615PMC
http://dx.doi.org/10.3390/biom12020184DOI Listing

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