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

Abstract

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.

Keywords: Dexpanthenol; apoptosis; inflammation; sepsis.

Graphical abstract

Figure 1.

DXP decreases the expressions of inflammatory cytokines in the serum of CLP-induced mice model. (a-d) Expressions of TNF-α, IL-1β, IL-6 and MCP-1 in the serum of mice was detected by ELISA. ***P < 0.001 vs Control; ^###P < 0.001 vs CLP.

Figure 2.

DXP reduces CLP-induced damage of kidney function, inflammation and pathological tissue in mice. (a-b) Biochemical kits were used to detect the expressions of kidney function indicators BUN and Cre in the serum of mice. (c) Expressions of NGAL and Kim1 in kidney tissues was assayed adopting western blot. (d) Expressions of TNF-α, IL-1β, IL-6 and MCP-1 in kidney tissues of mice was examined applying western blot. (e) Kidney histopathological damage was observed using HE staining. ***P < 0.001 vs Control; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 vs CLP.

Figure 3.

DXP reduces CLP-induced apoptosis in the kidney tissue of mice. (a) Level of apoptosis in the kidney tissues of mice was observed using TUNEL staining. (b-c) Expressions of apoptosis-related proteins in kidney tissues of mice were examined with the application of western blot. ***P < 0.001 vs Control; ^###P < 0.001 vs CLP.

Figure 4.

DXP reduces CLP-induced damage of liver function, inflammation, antioxidant enzymes and pathological tissue of mice. (a-c) Biochemical kits were used to assay liver function impairment indicators ALT, AST, ALP. (d) Assay of MPO activity in the liver of mice was undertaken using MPO kit. (e) Expressions of inflammatory factors TNF-α, IL-1β, IL-6, and MCP-1 in the liver tissues of mice were tested employing western blot. (f-g) Expressions of GSH and SOD in liver tissues of mice were measured using GSH and SOD kits. (h-i) Observation of liver histopathological damage in mice was conducted adopting HE staining. ***P < 0.001 vs Control; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 vs CLP.

Figure 5.

DXP reduces CLP-induced apoptosis in the liver of mice. (a) Measurement of apoptosis level in the hepatocytes of mice was carried out using TUNEL staining. (b-c) Detection of apoptosis-related protein expressions in the liver tissues of mice through western blot. ***P < 0.001 vs Control; ^#P < 0.05, ^###P < 0.001 vs CLP.