Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

Sepsis is capable of causing systemic infections resulting in multiple organ damage. Dexpanthenol (DXP) has been reported to protect against kidney and liver injury. Therefore, this paper attempts to explore the role of DXP in sepsis-induced kidney and liver injury. A mice model of sepsis was established using the cecal ligation and puncture (CLP) method. The expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and monocyte chemoattractant protein (MCP)-1 in the serum of mice were measured utilizing enzyme linked immunosorbent assay (ELISA). Additionally, the damage of kidney and liver tissues in CLP-induced mice was determined by their respective commercial kits, western blot, and hematoxylin-eosin (HE) staining kits. The apoptosis of kidney and liver tissues in CLP-induced mice was assessed by means of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and western blot. It was observed that DXP decreased the expressions of TNF-α, IL-1β, IL-6, and MCP-1 in the serum of CLP-induced mice, attenuated the functional impairment, pathological damage, inflammation, and cell apoptosis of kidney tissue. Meanwhile, DXP decreased the functional impairment of liver in CLP-induced mice, reduced the levels of inflammatory factors and antioxidant enzymes, attenuated liver pathological damage, and decreased cell apoptosis in liver tissues. In conclusion, DXP attenuates inflammatory damage and apoptosis in kidney and liver organs in a sepsis model.