International urogynecology journal · 2026
Alpha-Linolenic Acid and Tarantula Cubensis Extract Attenuate Bladder Inflammation in Cyclophosphamide-Induced Cystitis: A Comparative Experimental Study.
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Yıldız Mehmet, Batur Ali Furkan, Ateş Mehmet Burak, Bulut Ayşegül, Altintaş Emre, Gül Murat, Kaynar Mehmet, Kiliç Özcan, Göktaş Serdar
Аннотация
INTRODUCTION AND HYPOTHESIS: Primary bladder pain syndrome (PBPS) is a chronic inflammatory bladder disorder characterized by pelvic pain, urinary urgency, and frequency. Current intravesical therapies such as hyaluronic acid (HA) mainly restore the urothelial barrier but may not adequately address inflammatory and oxidative mechanisms underlying bladder injury. We investigated whether alpha-linolenic acid (ALA) and Tarantula cubensis extract (TCAE) provide greater protection than intravesical HA in an experimental cystitis model.
METHODS: Forty female Wistar rats were randomly assigned to five groups: control, cyclophosphamide (CYP)-induced cystitis, CYP + HA, CYP + TCAE, and CYP + ALA. Chemical cystitis was induced with intraperitoneal CYP (75 mg/kg). HA was administered intravesically, TCAE intraperitoneally, and ALA orally. Bladder tissues were evaluated using histopathological scoring and biochemical analyses measuring IL-6, TNF-α, SOD1, malondialdehyde [MDA]), and nerve growth factor-β (NGF-β).
RESULTS: CYP administration produced marked bladder injury characterized by epithelial degeneration, submucosal edema, inflammatory infiltration, fibrosis, and increased mast cell density. Both ALA and TCAE improved these histopathological alterations compared with untreated cystitis. The greatest recovery was observed in the ALA group. Tissue MDA levels differed significantly among groups, with the lowest values observed in the ALA group. In contrast, IL-6, TNF-α, SOD1, and NGF-β levels showed group-related trends but did not reach statistical significance.
CONCLUSIONS: ALA and TCAE attenuated bladder injury in this experimental cystitis model, with ALA demonstrating the most pronounced histological and antioxidative effects. These findings support further investigation of ALA as a potential therapeutic strategy in experimental bladder inflammation.
METHODS: Forty female Wistar rats were randomly assigned to five groups: control, cyclophosphamide (CYP)-induced cystitis, CYP + HA, CYP + TCAE, and CYP + ALA. Chemical cystitis was induced with intraperitoneal CYP (75 mg/kg). HA was administered intravesically, TCAE intraperitoneally, and ALA orally. Bladder tissues were evaluated using histopathological scoring and biochemical analyses measuring IL-6, TNF-α, SOD1, malondialdehyde [MDA]), and nerve growth factor-β (NGF-β).
RESULTS: CYP administration produced marked bladder injury characterized by epithelial degeneration, submucosal edema, inflammatory infiltration, fibrosis, and increased mast cell density. Both ALA and TCAE improved these histopathological alterations compared with untreated cystitis. The greatest recovery was observed in the ALA group. Tissue MDA levels differed significantly among groups, with the lowest values observed in the ALA group. In contrast, IL-6, TNF-α, SOD1, and NGF-β levels showed group-related trends but did not reach statistical significance.
CONCLUSIONS: ALA and TCAE attenuated bladder injury in this experimental cystitis model, with ALA demonstrating the most pronounced histological and antioxidative effects. These findings support further investigation of ALA as a potential therapeutic strategy in experimental bladder inflammation.