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Article Effectiveness of Boric Acid in Sepsis in Rats With Cecal Perforation(Springer Nature, 2025) Kurtipek, Ali Can; Dursun, Ali Dogan; Yigman, Zeynep; Ozdemir, Cagri; Kucuk, Aysegul; Gonullu, Ugur; Arslan, MustafaIntroduction and AimSepsis is a systemic inflammatory response that develops in the host against microorganisms, which results in end-organ damage. Boric acid (BA) has been shown to have immune modulatory effects in vitro and in animal studies. The aim of the study is to investigate the effects of high dose BA on lung and kidney tissues in rats with sepsis induced by the CLP method.Method28 rats were randomly divided into four groups: Group C (control group), Group BA, Group CLP (cecal ligation and puncture), and Group CLP + BA. Cecum was ligated below the ileocecal valve and punctured. BA was administered to the treatment groups at an intraperitoneal dose of 200 mg/kg, and at the end of 24 h, lung and kidney tissue samples were collected and evaluated for biochemical and histopathological parameters.ResultsHistopathologically, in kidney tissue, CLP + BA group showed significantly less peritubular capillary dilatation and brush border loss in the proximal tubule epithelium compared to the CLP group. In lung tissue, CLP + BA group had significantly less alveolar wall thickening compared to the CLP group. Biochemical analyses indicated that BA administration reduced oxidative stress in both renal and lung tissues.ConclusionWe found that intraperitoneal administration of high dose boric acid partially ameliorated the tissue damage in rats subjected to CLP induced sepsis. Further studies are needed regarding the dosage and application at different time points.Article Citation - WoS: 1Citation - Scopus: 2Cannabinoid Receptor Ligands Modulate Fibrosis and Inflammation in Idiopathic Pulmonary Fibrosis: a Preliminary Study(Tubitak Scientific & Technological Research Council Turkey, 2024) Kose, Sevil; Onen, Selin; Gizer, Merve; Boduroglu, Esin; Gonullu, Ugur; Korkusuz, PetekBackground/aim: No specific pharmacological treatment regimen for idiopathic pulmonary fibrosis (IPF) exists. Therefore, new antiinflammatory therapeutic strategies are needed. Cannabinoids (CBs), known for their inflammation-modulating and antifibrotic effects, may be potential medication candidates for treating IPF. We aim to evaluate the inflammation-modulating and antifibrotic effects of CB receptor (CBR) agonists and antagonists in lipopolysaccharide-stimulated normal human lung fibroblast, epithelial cells, IPF fibroblast cells, and monocytes. Materials and methods: We detected CBRs in normal human lung fibroblasts (LL24) and IPF fibroblast cells (LL29), epithelial cells (A549) and monocytes (THP-1) by flow cytometry. We determined TGF-(31, IL-8, and TNF-alpha inflammatory cytokines in the LL24, LL29, A549, and THP-1 cell culture supernatants on days 1 and 5 by ELISA. We evaluated the cell viability in LL24, LL29, and A549 cells on days 1, 3, and 5 spectrophotometrically and detected collagen Type I (ColI) production in the LL24 and LL29 cell culture supernatants on days 1, 3, and 5 by ELISA. Results: LL24, LL29, A549, and THP-1 cells exhibited CB1 (CB1R) and CB2 (CB2R) receptors. CB1R and CB2R agonists WIN55,2122 and JWH015 inhibited fibroblastic and epithelial cell proliferation on day 5. TGF-(31 and TNF-alpha release increased, while IL-8 release decreased in LL24, LL29, A549, and THP-1 cells in response to the administration of WIN55,212-2 and JWH015 at a 10-2 mM concentration. CB1R and CB2R antagonists AM251 and AM630 did not block agonistic responses, suggesting a nonclassical CBRmediated pathway. CB2R agonist JWH015 decreased ColI expression in IPF lung fibroblasts LL29 on day 3. Conclusion: These results suggest that CB signaling regulates the progression of pulmonary inflammation and fibrosis via CBR activation. This may offer a potential pharmacological tool for developing antifibrosis therapies.
