1. Sodium Thiosulfate Ameliorates Renovascular Hypertension-Induced Renal Dysfunction and Injury in Rats
- Author
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Shiu Dong Chung, Pei Li Chou, Sam Chi Lin, Chiang Ting Chien, and Yin Shian Chen
- Subjects
Male ,lcsh:Diseases of the circulatory (Cardiovascular) system ,renovascular hypertension ,Antioxidant ,medicine.medical_treatment ,Thiosulfates ,Blood Pressure ,Pharmacology ,lcsh:RC870-923 ,Kidney ,medicine.disease_cause ,Antioxidants ,Renovascular hypertension ,Fibrosis ,lcsh:Dermatology ,Animals ,Medicine ,Rats, Wistar ,chemistry.chemical_classification ,sodium thiosulfate ,Reactive oxygen species ,NADPH oxidase ,biology ,business.industry ,apoptosis ,General Medicine ,lcsh:RL1-803 ,lcsh:Diseases of the genitourinary system. Urology ,medicine.disease ,Oxidative Stress ,Hypertension, Renovascular ,Blood pressure ,chemistry ,lcsh:RC666-701 ,Nephrology ,Apoptosis ,biology.protein ,Reactive Oxygen Species ,Cardiology and Cardiovascular Medicine ,business ,Oxidative stress - Abstract
Background/Aims: Arterial stenosis activates the renin-angiotensin-aldosterone system subsequently resulting in renovascular hypertension (RVHT) and renal oxidative injury. We explored the effect of sodium thiosulfate (STS, Na2S2O3), a developed antioxidant in clinical trial, on RVHT-induced hypertension and renal oxidative injury in rats. Methods: We induced RVHT in male Wistar rats with bilaterally partial ligation of renal arteries in the 2-kidney 2-clip model. We evaluated the STS effect on RVHT-induced oxidative injury and apoptosis by a chemiluminescence amplification method, Western blot, and immunohistochemistry. Results: We found STS displayed a dose-dependent antioxidant H2O2 activity and adapted the maximal scavenging H2O2 activity of STS at the dosage of 0.1 g/kg intraperitoneally 3 times/week for 4 weeks in RVHT rats. RVHT induced a significant elevation of arterial blood pressure, blood reactive oxygen species amount, neutrophil infiltration, 4-HNE and NADPH oxidase gp91 expression, Bax/Bcl-2/poly(ADP-ribose) polymerase (PARP)-mediated apoptosis formation, blue Masson-stained fibrosis, and urinary protein level. STS treatment significantly reduced hypertension, oxidative stress, neutrophil infiltration, fibrosis, and Bax/Bcl-2/PARP-mediated apoptosis formation and depressed the urinary protein level in the RVHT models. Conclusion: Our results suggest that STS treatment could ameliorate RVHT hypertension and renal oxidative injury through antioxidant, antifibrotic, and antiapoptotic mechanisms.
- Published
- 2020