Bleomycin (BLM) is a chemotherapeutic agent that can cause pulmonary fibrosis. Little is known about the possible protective role of the CB2 receptor agonist, AM1241. We investigated the effects of CB2 receptor activation by AM1241 on BLM induced lung fibrosis in a rat model. BLM was administered via the trachea. Adult female Wistar rats were divided into five groups: saline (control group), BLM (BLM group), CB2 agonist (AM1241) + BLM (BLMA group), CB2 antagonist (AM630) and CB2 agonist (AM1241) + BLM (BLMA + A group), and vehicle (dimethylsulfoxide) + BLM (BLM + vehicle group). Hydroxyproline, collagen type 1, total protein, glutathione (GSH), malondialdehyde (MDA), interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels were measured in lung fibrosis and control tissue using standard methods. We investigated the histopathology of lung tissue to determine the extent of fibrosis. We found significantly higher levels of hydroxyproline, TNF-α, IL-6 and total protein in the BLM group compared to the BLMA group. The level of GSH also was higher in the BLMA group compared to the BLM group. Inflammation and fibrotic changes were significantly reduced in the BLMA group. Our findings suggest that CB2 receptor activation provided protection against BLM induced pulmonary fibrosis by suppressing oxidative stress and increasing cytokines.

We investigated the effects of α-lipoic acid (AL) and α-tocopherol (AT) on renal histopathology in a streptozotocin (STZ) induced diabetic rat model. Adult male rats were divided into six groups: group 1, saline only; group 2, AL only; group 3, AT only; group 4, STZ only; group 5, STZ + AL; group 6 STZ + AT. Experimental diabetes was induced by STZ. AL and AT were administered for 15 days. Kidney sections were examined using a light microscope after hematoxylin and eosin (H & E), periodic acid-Schiff (PAS) and caspase-3 staining. Histological damage to glomeruli, tubule epithelial cells and basement membrane was observed in group 4. Administration of AT and AL reduced renal injury in the diabetic rats. Group 5 exhibited a greater curative effect on diabetic rats than group 6. AT and AL may be useful for preventing diabetic renal damage.

Background/Objectives: The aim of this study was to compare the biochemical, histological, immunohistochemical and ultrastructural hepatic phenotypes associated with carbohydrate-, fat- and protein-enriched diets initiated during post-weaning growth. Methods: Forty 21-day-old male Wistar albino rats were divided into four groups: a control group and three experimental groups (carbohydrate, protein, and fat). The respective diets were fed for 13 weeks. Hepatic oxidant–antioxidant parameters, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), histopathological scores; interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) immunoreactivity and transmission electron microscopy (TEM) findings were evaluated. Results: The carbohydrate group showed higher thiobarbituric acid-reactive substances (TBARS), total oxidant status (TOS) and oxidative stress index (OSI), together with lower reduced glutathione (GSH) and total antioxidant status (TAS). Histology showed hydropic change, vacuolization and inflammatory cell infiltration, while TEM showed mitochondrial swelling, loss of cristae and nuclear alterations. The fat group showed prominent vacuolization, TEM-observed lipid droplets, inflammatory cell infiltration and TNF-α immunoreactivity. Most findings in the protein group were closer to control values. Thus, the carbohydrate-enriched diet was associated with the most pronounced redox and ultrastructural injury profile, whereas the fat-enriched diet was associated with a morphological and inflammatory injury profile compatible with lipid accumulation. Conclusions: These findings identify distinct hepatic phenotypes associated with the dietary formulations administered during post-weaning growth. The carbohydrate- and fat-enriched formulations were associated with more pronounced biochemical and morphological changes; inference is made at the level of the complete dietary formulation.

Background/Objectives: Bile duct ligation (BDL), characterized by marked inflammation and fibrosis, effectively mimics many clinical conditions and is a valuable tool for investigating biliary regeneration. Our objective was to clarify the therapeutic benefits of adipose-derived stem cell (ADSC) treatment and signaling pathways mediating regenerative processes in a rat model of BDL. Methods: The BDL model was performed on Sprague–Dawley rats, and ADSC was administered intrasplenically at a dose of 10⁶ cells per animal. Liver function tests, gene and protein expression analyses, histological evaluation, and immunohistochemistry staining were performed to assess liver function, signaling pathways, inflammation, and fibrosis. Results: ADSC treatment returned liver function to sham levels. ADSC upregulated the Hes1 gene and protein expression in the early and late term. Inflammation, fibrosis, and total damage scores were decreased following ADSC treatment compared with the control. Immunohistochemistry staining revealed higher CD90, CD44, and CD29 stem cell marker expression in the ADSC treatment group. Conclusions: ADSC administration reduced fibrosis and biliary damage and restored liver function, potentially in a manner mediated by upregulated Hes1 expression, supporting its promise in biliary regeneration.