The protective effect and mechanism of lentinan on acute kidney injury in septic rats

This study aimed to investigate the protective effect and mechanism of lentinan (LNT) on acute kidney injury (AKI) in septic rats.A total 72 male SD rats were randomly divided into 6 groups with 12 rats in each group. Except for the sham group, all groups, including the burn sepsis group (BS group), the positive drug control group (dexamethasone, 5 mg/kg, PC group), the LNT low-concentration group (LNT-L group) (50 mg/kg), the LNT medium-concentration group (LNT-M group) (100 mg/kg), and the LNT high-concentration group (LNT-H group) (200 mg/kg), were intraperitoneally injected with the same amount of normal saline 30 min before injury. The levels of serum interleukin (IL)-4, IL-6, IL-10, and tumor necrosis factor alpha (TNF-α); the indexes of blood urea nitrogen (BUN) and creatinine (Cr); and the protein expression levels of inducible nitric oxide synthase (iNOS), intercellular adhesion molecule 1 (ICAM-1), and nuclear factor-κB (NF-κB) in renal tissue were detected 24 hours after the model was established.Compared with the sham group, the BUN and Cr of the other groups were significantly higher, while those of the LNT group with different concentrations were significantly lower than those of the BS group (P<0.05). Compared with the sham group, the protein expression levels of NF-κB, iNOS, and ICAM-1 along with the levels of pro-inflammatory factors TNF-α and IL-6 in serum were significantly increased, while the levels of anti-inflammatory factors IL-4 and IL-10 were obviously lower in the BS group. Compared with the BS group, the protein expression levels of NF-κB, iNOS, and ICAM-1 along with the levels of pro-inflammatory factors TNF-α and IL-6 in serum were significantly decreased, while the levels of anti-inflammatory factors IL-4 and IL-10 were obviously increased in the LNT group with different concentrations..LNT has a certain protective effect on AKI in septic rats, and its mechanism may involve inhibiting the activation of NF-κB, which suppresses the expression of proinflammatory factors in turn, thus promoting the release of anti-inflammatory factors.