Fig 1: Effects of SA on oxidative stress parameters in LPS‐induced AKI in rats. Serum TAS (a), TOS (b), OSI (c), SOD (e), and GPx (f) levels and renal MDA (d) levels were evaluated in the control, LPS, and LPS + SA groups. Data are presented as mean ± SD (n = 8 per group). Statistical analysis was performed using the Kruskal–Wallis H test followed by the Mann–Whitney U test. p values are indicated in the graphs. LPS administration significantly increased TOS, OSI, and renal MDA levels compared with the control group. SA pretreatment significantly attenuated the LPS‐induced increase in renal MDA but did not significantly alter SOD, GPx, or TAS. These findings indicate a selective reduction in lipid peroxidation rather than a generalized enhancement of antioxidant defenses. GPx, glutathione peroxidase; LPS, lipopolysaccharide; MDA, malondialdehyde; OSI, oxidative stress index; SA, Sinapic acid; SOD, superoxide dismutase; TAS, total antioxidant status; TOS, total oxidant status.
Fig 2: Experimental design and timeline for evaluating the protective effects of SA against LPS‐induced AKI in rats. Rats were orally pretreated with SA (40 mg/kg/day) for 7 consecutive days. On Day 7, LPS (5 mg/kg) was administered intraperitoneally to induce AKI. On Day 7, 2 h after the final SA dose, LPS was administreted intraperitoneally. Rats were monitored, and at 6 h post‐injection, all animals were sacrificed for tissue and blood collection. Histopathological evaluation of kidney tissues was performed to assess tubular injury scores. Immunohistochemistry was conducted to detect Beclin‐1 (autophagy marker), TNF‐α (inflammation marker), and Caspase‐3 (apoptosis marker). Blood samples were analyzed for biochemical markers, including CREA, ALB, TP, BUN, UA, and SQSTM1/p62 (autophagy‐related marker). Oxidative stress parameters, including MDA, SOD, GPx, TAS, and TOS, were quantified in kidney tissues to evaluate the redox balance. AKI, acute kidney injury; ALB, albumin; BECN1, Beclin‐1; BUN, blood urea nitrogen; CREA, creatinine; GPx, glutathione peroxidase; LDH, lactate dehydrogenase; LPS, lipopolysaccharide; MDA, malondialdehyde; SA, Sinapic acid; SOD, superoxide dismutase; SQSTM1, sequestosome 1; TAS, total antioxidant status; TNF‐α, tumor necrosis factor‐alpha; TOS, total oxidant status; TP, total protein; UA, uric acid. Created in BioRender. Okuyan, H. M. (2026) https://BioRender.com/ggmmyv2.
Fig 3: Effects of SA on circulating SQSTM1/p62 levels in rats with LPS‐induced AKI. LPS administration significantly increased serum SQSTM1 levels compared with the control group (p < 0.001), whereas SA pretreatment significantly attenuated this increase (p < 0.001). Serum SQSTM1 was evaluated as an autophagy‐related marker and not as a direct measure of renal autophagic flux. Data are presented as mean ± SD (n = 8 per group). Statistical analysis was performed using the Kruskal–Wallis H test followed by the Mann–Whitney U test. LPS, lipopolysaccharide; SA, Sinapic acid; SQSTM1, sequestosome 1.
Supplier Page from Fine Biotech Co., Ltd. for Rat SQSTM1 (Sequestosome-1) ELISA Kit