Rosmarinic acid attenuated inflammation and apoptosis in folic acid-induced renal injury: Role of FoxO۳/ NFκB pathway

سال انتشار: 1404
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 290

فایل این مقاله در 7 صفحه با فرمت PDF قابل دریافت می باشد

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این مقاله:

شناسه ملی سند علمی:

JR_IJBMS-28-3_006

تاریخ نمایه سازی: 23 دی 1403

چکیده مقاله:

Objective(s): Rosmarinic acid (RA) is a herbal compound with various antioxidant and anti-inflammatory effects. This study aimed to explore the anti-inflammatory and anti-apoptotic properties of RA in folic acid-induced renal injury.Materials and Methods: Thirty-six male C۵۷/BL۶ mice were randomly divided into six groups (N=۶): Control (received normal saline), NaHCO۳ (received NaHCO۳ as folic acid solvent), FA (received folic acid (FA)(IP) to induce renal injury), RA (received ۱۰۰ mg/kg RA), RA۵۰-FA (received ۵۰ mg/kg RA solution after folic acid injection), and RA۱۰۰-FA (received ۱۰۰ mg/kg RA after folic acid injection). For ten days, the treatment groups received RA by gavage. The effects of RA were assessed using H & E staining, biochemical tests, western blotting, and ELISA in the kidney tissues of the mice. Real-time RT-PCR was also performed to evaluate the expression changes of renal genes.Results: Our data showed that treatment by RA led to the over-expression of FoxO۳ (P<۰.۰۵) and decrease in NFκB levels (P<۰.۰۱ and P<۰.۰۵) and expression of TNFα (P<۰.۰۵) and IL۶ (P<۰.۰۰۱ and P<۰.۰۱). Other evaluations showed a decrease in p۵۳ (P<۰.۰۱ and P<۰.۰۰۱), Bax/Bcl-۲ ratio expression (P<۰.۰۱ and P<۰.۰۵), and Caspase-۳ level (P<۰.۰۱ and P<۰.۰۵) compared to the folic acid group. Histological and biochemical results also confirmed the attenuation of tissue damage.Conclusion: This study revealed that RA’s positive effects on folic acid-induced renal injury might result from the involvement of the FoxO۳/NFκB pathway, thereby suppressing inflammation and apoptosis.

نویسندگان

Maryam Mottaghi

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

Fatemeh Heidari

Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran

Tahereh Komeili Movahhed

Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran

Akram Eidi

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

Azam Moslehi

Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran

مراجع و منابع این مقاله:

لیست زیر مراجع و منابع استفاده شده در این مقاله را نمایش می دهد. این مراجع به صورت کاملا ماشینی و بر اساس هوش مصنوعی استخراج شده اند و لذا ممکن است دارای اشکالاتی باشند که به مرور زمان دقت استخراج این محتوا افزایش می یابد. مراجعی که مقالات مربوط به آنها در سیویلیکا نمایه شده و پیدا شده اند، به خود مقاله لینک شده اند :
  • Lamprea-Montealegre JA, Joshi P, Shapiro AS, Madden E, Navarra K, ...
  • Yan LJ. Folic acid-induced animal model of kidney disease. Animal ...
  • Zadarko-Domaradzka M, Kruszyńska E, Zadarko E. Effectiveness of folic acid ...
  • Srivastava SP, Kanasaki K, Goodwin JE. Loss of mitochondrial control ...
  • Xu S, Zhang X, Ma Y, Chen Y, Xie H, ...
  • Jiang WL, Xu Y, Zhang SP, Hou J, Zhu HB. ...
  • Marinho S, Illanes M, Ávila-Román J, Motilva V, Talero E. ...
  • Lu B, Li C, Jing L, Zhuang F, Xiang H, ...
  • Gao Y, Wang C, Jiang D, An G, Jin F, ...
  • Domitrović R, Potočnjak I, Crnčević-Orlić Z, Škoda M. Nephroprotective activities ...
  • Kuypers FA. Hyperinflammation, apoptosis, and organ damage. Exp Biol Med ...
  • نمایش کامل مراجع