Fig 2: Effect of CCJ12 on C-reactive protein. Plasma C-reactive protein was measured as described in “Materials and Methods”. CG, a control diet; FG, a high fat diet, FCG, a high fat diet with CCJ12. The data was analyzed using one-way ANOVA with Holm-Sidak method and the difference of CRP levels was found insignificant between the groups. Data is detonated as the mean ± SD (n = 10).

Fig 3: Experimental design and evaluated parameters in the FIP-induced sepsis model. A total of four groups were established: control (Group 1), feces-induced peritonitis (FIP, Group 2), FIP + Saline (Group 3), and FIP + MB (20 mg/kg, Group 4). FIP was induced via intraperitoneal fecal slurry administration. One hour after induction, MB was administered intraperitoneally to Group 4. All evaluations were conducted at the 24th hour post-induction. Biochemical markers (MDA, CRP, IL-1β, IL-6, TNF-α, lactic acid, cGMP), histopathological parameters (alveolar congestion, hemorrhage, neutrophil infiltration, alveolar wall thickening, pulmonary edema), radiological lung density via Hounsfield unit (HU) on CT, and arterial blood gas (PaO2 and PaCO2) measurements were performed.

Fig 4: Biochemical alterations in FIP-induced lung injury and modulation by MB. (A–E) MDA, TNF-α, CRP, lactic acid, and cGMP levels were significantly increased in the FIP and FIP + Saline groups versus control, reflecting oxidative stress, inflammation, metabolic disturbance, and vascular activation. MB significantly reduced all markers. No significant differences were found between FIP and FIP + Saline groups. Data are mean ± SEM (n = 10). One-way ANOVA followed by Tukey’s post hoc test for MDA, CRP, and cGMP; Tamhane’s T2 for TNF-α and lactic acid. ns: not significant; * p < 0.05; ** p < 0.01; *** p < 0.001.