Fig 1: The cellular mechanism of damage to the liver due to acute poisoning of CCl4. The effect of toxic metabolite CCl4 (●CCl3) on Hepatocytes and Kupffer cells, and the effect of NGAL on the deterioration of the inflammatory reaction in the liver.
Fig 2: The effect of treatment on renal injuryMarkers of renal injury following treatment with vehicle, sunitinib (14 mg/kg/day; SU) alone or during co-treatment with low-dose aspirin (COX-1 inhibition, 5 mg/kg/day; SU+low-dose A) or high-dose aspirin (dual COX-1 and COX-2 inhibition, 100 mg/kg/day; SU+high-dose A) in WKY rats. (A) Albuminuria, the renal mRNA expression of (B) nephrin and (C) podocin and the urinary excretion of (D) NGAL and (E) KIM-1. Renal mRNA expression is normalised to the internal housekeeping gene, Hprt1, and is expressed relative to the vehicle-treated group. Data are presented as mean ± SEM (n=5–7/group). Data were analysed using a one-way ANOVA. *P<0.05 versus vehicle-treated.
Fig 3: Effect of CCl4 and bilberry fruit extract on histopathology of rat liver after 24 h (H&E and Immunohistochemical staining). I-group I (untreated group), II-group II (treated group), III-group III (CCl4), IV-group IV (treated + CCl4). (A) group I (untreated group), 100×; (B) group II (treated group), 100×; (C1–C11) group III (CCl4); C1-Necrosis followed by minor and severe reversible change, 100×; C2-Necrosis followed by macrovesicular hepatocytes, 100×; C3-Necrosis followed by vacuolar hepatocytes, 100×; C4-Hemorrhagic coagulation necrosis, 100×; C5-Necrosis (??), macrovesicular hepatocytes (?), hydropic hepatocytes (?), inflammatory mononuclear infiltrate (??), 200×; C6-Hemorrhagic coagulation necrosis (??), 200×; C7-Necrosis (??), vacuolar hepatocytes (?), 200×; C8- macrovesicular fatty hepatocytes (?), 400×; C9-Necrosis (??), microvesicular fatty hepatocytes (?), 400×; C10-Necrosis (??), 400×; C11-Inflammatory mononuclear infiltrate (??), 400×; (D1–D3) group IV (treated + CCl4); D1-minor reversible change (hydropic hepatocytes), 100×; D2- minor reversible change (vacuolar hepatocytes) and extended sinusoidal spaces, 200×; D3-Hydropic hepatocytes (?), 400×; (E) immunohistochemical detection of COX-2, 100×; (F) immunohistochemical detection of iNOS (NOS2), 100×; (G) immunohistochemical detection of TNF-a, 100×, (H) immunohistochemical detection of NGAL, 100×; (I) immunohistochemical detection Kupffer cells identification marker-CD68, 100×; (J) morphometric analysis extent of the necrotic area on a selected H&E field in the liver. The data show the average value ± S.D. (%) for 10 fields at the magnification of 200× for each animal in each group (H&E staining); (K) semiquantitative evaluation of COX-2, iNOS, TNF-a, NGAL, and CD68 immunohistochemistry staining. Staining intensity was graded as: - (negative), +/- (weak positive), + (positive), ++ (strongly positive), or +++ (very strongly positive).
Supplier Page from Abcam for Rat Lipocalin-2 ELISA Kit