Dysregulation of bile acid signal transduction causes neurological dysfunction in cirrhosis rats

Figure 1 Thioacetamide-induced bile acid feeding in cirrhotic rats led to increased anxiety-like behavior (mean ± SD, n = 10). A-D: The total distance of the open-field experiment, the number of central areas of the open open-field experiment, and the open arm of the elevated cross-experiment, percentage of entry times and percentage of residence time of open arm in elevated cross test. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. TAA: Thioacetamide.

Figure 2 Liver hepatic encephalopathy and liver biochemical indices (mean ± SD, n = 10). A: Hematoxylin and eosin staining of liver tissue of rats in each group (× 200); B and C: Serum aspartate aminotransferase and alanine aminotransferase indexes. Scale bar = 500 μm. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. TAA: Thioacetamide.

Figure 3 Serum and cerebral cortex total bile acid content (mean ± SD, n = 10). A: The content of total bile acid in serum; B: The total bile acid content in the cerebral cortex. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. TAA: Thioacetamide.

Figure 4 Comparison of serum and cerebral cortex neuroinflammatory factors in each group (mean ± SD, n = 10). A-C: The content comparison of interleukin-1β (IL-1β), IL-6, and IL-10 in serum of each group; D-F: Compares IL-1β, IL-6, and IL-10 in the cerebral cortex. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. IL: Interleukin; TAA: Thioacetamide.

Figure 5 Immunohistochemical results of expression of microglia activation marker ionized calcium-binding adaptor molecule-1 in cerebral cortex (mean ± SD, n = 10). A: Results of immunochemical staining of the cerebral cortex (× 200); B: Comparison of the expression level of ionized calcium-binding adaptor molecule-1 protein in the cerebral cortex of rats in the four groups. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. TAA: Thioacetamide; IBA-1: Ionized calcium-binding adaptor molecule-1.

Figure 6 Takeda G protein-coupled receptor 5 and ionized calcium-binding adaptor molecule-1 were measured by reverse transcription polymerase chain reaction (mean ± SD, n = 10). A and B: The expression of Takeda G protein-coupled receptor 5 and ionized calcium-binding adaptor molecule-1 in the cerebral cortex, respectively. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. TAA: Thioacetamide; TGR5: Takeda G protein-coupled receptor 5; IBA-1: Ionized calcium-binding adaptor molecule-1.

Figure 7 Western blot results of ionized calcium-binding adaptor molecule-1 and Takeda G protein-coupled receptor 5 protein expression in cerebral cortex of rats in each group (mean ± SD, n = 10). A: Protein expression bands of ionized calcium-binding adaptor molecule-1 and Takeda G protein-coupled receptor 5 in the cerebral cortex of thioacetamide-induced liver cirrhosis model with GADPH as the upper sample control; B and C: The expression of ionized calcium-binding adaptor molecule-1 and Takeda G protein-coupled receptor 5 protein in each group, respectively. ^aP < 0.05 compared with vehicle + control diet group; ^bP < 0.05 compared with thioacetamide group. TAA: Thioacetamide; TGR5: Takeda G protein-coupled receptor 5; IBA-1: Ionized calcium-binding adaptor molecule-1.