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Updated: Sep 20, 2026
Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
Published on: October 17, 2025
Evidence that dl-propranolol increases thymidine kinase activity, cell mitosis, and beta-adrenoceptors during rat
Verónica Reyes-Salcido1, Rafael Villalobos-Molina
1Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados-Sede Sur, Mexico City, Mexico.
Background:
Adrenoceptor stimulation has been described as an important factor in liver regeneration. We examined the effects of the beta-adrenoceptor antagonist, dl-propranolol, during early steps of regeneration after partial hepatectomy in rat.
Methods:
Thymidine kinase (TK) activity, cell mitosis, and beta-adrenoceptors were measured after a single intraperitoneal (i.p.) injection of dl-propranolol (10 mg/kg) immediately following 70% partial hepatectomy. Enzyme activity was measured as [3H] thymidine (dThd) monophosphate; mitotic index was determined after tissue staining, and beta-adrenoceptors were quantified by saturation binding of [3H] dihydroalprenolol. Liver regeneration was followed for 3 days.
Results:
dl-Propranolol increased TK activity as early as 12 h postsurgery, after which it leveled off at 24 h and declined at later times; mitotic index increased from 12 to 48 h after injection and beta-adrenoceptors augmented at 24 h compared to partial hepatectomy alone.
Conclusions:
dl-Propranolol up-regulated beta-adrenoceptors early after partial hepatectomy with an increase in TK activity and augmented hepatocyte mitosis. These data may suggest that dl-propranolol modulates, probably via beta-adrenoceptor blockade, early steps of liver regeneration.
