Document Type : Original Article
Authors
1
Medical physiology department, faculty of Medicine, Menoufia University
2
Medical Biochemistry and Molecular Biology Department, Faculty of medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
3
Clinical Pathology Department, National Liver Inistitute, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
4
4Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
5
Clinical Pharmacology Department, Faculty of medicine, Damitta University, Egypt
6
Anatomy and Embryology Department, Faculty of Medicine, Portsaid University, Portsaid, Egypt
7
Pathology Department, Faculty of Medicine, Menoufia University Shebin El-Kom, Menoufia, Egypt.
8
Internal Medicine and Nephrology department, Faculty of Medicine, Menoufia University Shebin El-Kom, Menoufia, Egypt.
9
Medical Physiology Department, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt
10
Medical Physiology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
Abstract
Background: It is becoming more well accepted that hyperuricemia may be a contributing factor to hypertension, renal illness, and a number of detrimental effects of vascular disease. It has been shown that albiflorin (ALB) has potent pharmacological effects in preventing oxidation, inflammation, and apoptosis.
Objective: to illustrate the underlying mechanisms and renoprotective impact of ALB in hyperuricemic rats.
Material & Methods: Thirty Wister albino male rats divided into control, HU, HU+ALB groups. After 8 weeks rats were subjected to arterial blood pressure (ABP), renal blood flow velocity (RBFV) and renal artery resistance (RAR) measurement and serum levels of urea, creatinine in addition to creatinine clearance, urinary protein, renal MDA, SOD, TNF-α, IL-6, renal genes expression of HMGB1, TLR4 and NF κB were assessed. Renal tissue was evaluated histopathologically and immunohistochemically.
Results: The measured SBP, DBP , MABP, RAR, serum levels of uric acid, urea, creatinine in addition to urinary protein, renal MDA, renal TNF-α, renal IL-6, renal genes HMGB1, TLR4 and NF-kB of HU group were dramatically increased compared to control however RBFV, renal SOD and creatinine clearance values of HU group were substantially decreased compared to control. In addition there were dramatically upregulated Bax and NF-kB immunoreaction of HU group compared to control. ALB significantly enhanced the alterations brought about by HU.
Conclusion: Through anti-oxidant, anti-inflammatory, and anti-apoptotic processes as well as the down-regulation of HMGB1, TLR4, and NF κB renal gene expression, ALB reduced HU-induced renal impairment
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