sinigrin and Kidney-Diseases

sinigrin has been researched along with Kidney-Diseases* in 1 studies

Other Studies

1 other study(ies) available for sinigrin and Kidney-Diseases

Article	Year
Sinigrin attenuates angiotensin II‑induced kidney injury by inactivating nuclear factor‑κB and extracellular signal‑regulated kinase signaling International journal of molecular medicine, 2021, Volume: 48, Issue:2 The present study investigated the function of sinigrin in angiotensin II (Ang II)‑induced renal damage. The results demonstrated that systolic blood pressure (SBP) and diastolic blood pressure (DBP) were increased in Ang II‑challenged rats, and sinigrin treatment inhibited their increase. The levels of blood urea nitrogen (BUN) and serum creatinine (SCR) were increased by Ang II in the rats, and these were reversed by sinigrin in a dose‑dependent manner. In addition, the Ang II‑induced elevation of urinary protein levels was inhibited by sinigrin treatment. Glomerular basement membrane thickness and ECM degradation markers, such as collagen I, collagen IV and fibronectin, were suppressed by sinigrin in the Ang II‑challenged rats. Moreover, the levels of inflammatory regulators, including tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6) and monocyte chemoattractant protein‑1 (MCP‑1), were reduced following sinigrin treatment of the Ang II‑challenged rats and in Ang II‑exposed proximal tubule epithelial cells. Furthermore, the superoxide dismutase (SOD) and catalase (CAT) levels were downregulated, whereas the malondialdehyde (MDA) levels were upregulated by Ang II; these effects were reversed by sinigrin treatment Topics: Angiotensin II; Animals; Cell Line; Chemokine CCL2; Creatinine; Gene Expression Regulation; Glucosinolates; Humans; Inflammation; Kidney; Kidney Diseases; Malondialdehyde; MAP Kinase Signaling System; NF-kappa B; Oxidative Stress; Rats, Inbred SHR; Rats, Sprague-Dawley; Superoxide Dismutase; Tumor Necrosis Factor-alpha	2021

Article

Year

Sinigrin attenuates angiotensin II‑induced kidney injury by inactivating nuclear factor‑κB and extracellular signal‑regulated kinase signaling

International journal of molecular medicine, 2021, Volume: 48, Issue:2

The present study investigated the function of sinigrin in angiotensin II (Ang II)‑induced renal damage. The results demonstrated that systolic blood pressure (SBP) and diastolic blood pressure (DBP) were increased in Ang II‑challenged rats, and sinigrin treatment inhibited their increase. The levels of blood urea nitrogen (BUN) and serum creatinine (SCR) were increased by Ang II in the rats, and these were reversed by sinigrin in a dose‑dependent manner. In addition, the Ang II‑induced elevation of urinary protein levels was inhibited by sinigrin treatment. Glomerular basement membrane thickness and ECM degradation markers, such as collagen I, collagen IV and fibronectin, were suppressed by sinigrin in the Ang II‑challenged rats. Moreover, the levels of inflammatory regulators, including tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6) and monocyte chemoattractant protein‑1 (MCP‑1), were reduced following sinigrin treatment of the Ang II‑challenged rats and in Ang II‑exposed proximal tubule epithelial cells. Furthermore, the superoxide dismutase (SOD) and catalase (CAT) levels were downregulated, whereas the malondialdehyde (MDA) levels were upregulated by Ang II; these effects were reversed by sinigrin treatment

Topics: Angiotensin II; Animals; Cell Line; Chemokine CCL2; Creatinine; Gene Expression Regulation; Glucosinolates; Humans; Inflammation; Kidney; Kidney Diseases; Malondialdehyde; MAP Kinase Signaling System; NF-kappa B; Oxidative Stress; Rats, Inbred SHR; Rats, Sprague-Dawley; Superoxide Dismutase; Tumor Necrosis Factor-alpha

2021