Ketogal Safety Profile in Human Primary Colonic Epithelial Cells and in Mice.
Federica SodanoBice AvalloneMonica TizzanoChiara FoglianoBarbara RolandoElena GazzanoChiara RigantiSalvatore MaglioccaMariarosaria CuozzoStefania AlbrizioAntonio CalignanoClaudia CristianoRoberto RussoMaria Grazia RimoliPublished in: Pharmaceuticals (Basel, Switzerland) (2021)
In our previous studies, a ketorolac-galactose conjugate (ketogal) showed prolonged anti-inflammatory and analgesic activity, causing less gastric ulcerogenic effect and renal toxicity than its parent drug ketorolac. In order to demonstrate the safer profile of ketogal compared to ketorolac, histopathological changes in the small intestine and liver using three staining techniques before and after repeated oral administration in mice with ketorolac or an equimolecular dose of its galactosylated prodrug ketogal were assessed. Cytotoxicity and oxidative stress parameters were evaluated and compared in ketorolac- and ketogal-treated Human Primary Colonic Epithelial cells at different concentrations and incubation times. Evidence of mitochondrial oxidative stress was found after ketorolac treatment; this was attributable to altered mitochondrial membrane depolarization and oxidative stress parameters. No mitochondrial damage was observed after ketogal treatment. In ketorolac-treated mice, severe subepithelial vacuolation and erosion with inflammatory infiltrates and edematous area in the intestinal tissues were noted, as well as alterations in sinusoidal spaces and hepatocytes with foamy cytoplasm. In contrast, treatment with ketogal provided a significant improvement in the morphology of both organs. The prodrug clearly demonstrated a safer profile than its parent drug both in vitro and ex vivo, confirming that ketogal is a strategic alternative to ketorolac.
Keyphrases
- oxidative stress
- ischemia reperfusion injury
- endothelial cells
- diabetic rats
- anti inflammatory
- type diabetes
- high fat diet induced
- gene expression
- adipose tissue
- replacement therapy
- combination therapy
- drug induced
- spinal cord
- adverse drug
- skeletal muscle
- ulcerative colitis
- wild type
- insulin resistance
- liver injury
- heat stress
- endoplasmic reticulum stress