To discuss the effect of baicalin on renal injury in nephrotic syndrome (NS) rats by regulating the high mobility group protein B1 (HMGB1)/Toll like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway.

SD rats were divided into control group, model group, experimental group, HMGB1 inhibitor group and HMGB1 activator group, with 12 rats in each group. Except for the control group, rats in all other groups were injected with adriamycin via the tail vein to establish the nephrotic syndrome (NS) model. Twenty-four hours after successful modeling, the rats in the experimental group were administered 100 mg·kg^-1 baicalin by gavage; rats in the HMGB1 inhibitor group were administered 0.03 g·kg^-1 HMGB1 inhibitor glycyrrhizic acid by gavage; rats in the HMGB1 activator group were administered 100 mg·kg^-1 baicalin by gavage combined with intraperitoneal injection of 8 μg·kg^-1 HMGB1 activator recombinant HMGB1 protein (rHMGB1); rats in the model group and control group were administered 10 mL·kg^-1 normal saline by gavage and intraperitoneal injection. All treatments were administered once daily for 30 consecutive days. Measure 24-hour urinary protein, serum creatinine, blood urea nitrogen levels, renal pathology, and renal levels of interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α). TUNEL staining was used to detect the apoptosis rate of cells in renal tissue. Western blot was used to detect renal caspase-3, p53, HMGB1, TLR4, and p-NF-κB p65 proteins.

In the model group, the renal tissue showed thickening of the glomerular basement membrane, glomerular atrophy, and extensive inflammatory cell infiltration; the 24 h urinary protein levels in the control group, model group, experimental group, HMGB1 inhibitor group, and HMGB1 activator group were (65.56±4.73), (212.19±12.26), (87.76±5.15), (95.53±6.11) and (138.87±8.25) mg·24 h^-1, respectively; the serum creatinine levels were (51.57±3.18), (128.86±7.25), (63.69±4.12), (70.75±4.06) and (95.73±5.29) μmol·L^-1, respectively; the serum blood urea nitrogen levels were (4.23±0.25), (10.68±0.61), (5.44±0.32), (6.18±0.39) and (8.78±0.53) mmol·L^-1, respectively; the renal tissue IL-1β levels were (37.65±2.18), (83.39±5.07), (44.55±2.56), (50.52±2.89) and (69.89±4.17) pg·mL^-1, respectively; the renal tissue MCP-1 levels were (156.69±8.12), (314.45±17.36), (181.54±10.21), (201.16±11.54) and (264.45±14.58) pg·mL^-1, respectively; the renal tissue TNF-α levels were (34.99±2.15), (90.81±5.63), (43.78±2.52), (51.19±3.15) and (67.11±3.89) pg·mL^-1, respectively; the renal tissue apoptosis rates were (4.67±0.31)%, (28.81±1.76)%, (7.08±0.39)%, (8.26±0.51)% and (18.22±1.03)%, respectively; the renal tissue Caspase-3 protein expression levels were 0.86±0.10, 2.37±0.16, 0.98±0.09, 1.21±0.18 and 1.85±0.17, respectively; the renal tissue tumor protein p53 (p53) protein expression levels were 0.15±0.02, 0.68±0.07, 0.24±0.03, 0.36±0.04 and 0.51±0.05, respectively; the renal tissue HMGB1 protein expression levels were 0.65±0.08, 2.04±0.17, 0.87±0.09, 0.95±0.08 and 1.34±0.13, respectively; the renal tissue TLR4 protein expression levels were 0.41±0.05, 1.68±0.16, 0.63±0.07, 0.79±0.08 and 1.09±0.11, respectively; the renal tissue p-NF-κB p65 protein expression levels were 0.23±0.03, 0.81±0.09, 0.37±0.05, 0.45±0.04 and 0.68±0.07, respectively. All differences between the control group and the model group, between the model group and the experimental group/HMGB1 inhibitor group, and between the experimental group and the HMGB1 activator group were all statistically significant (all P<0.05).

Baicalin may inhibit the inflammatory response and cell apoptosis in NS rats, and alleviate renal injury by suppressing HMGB1/TLR4/NF-κB pathway.