In this blog, I want to discuss the anti-inflammatory benefits of Fucoidan and diabetic nephropathy.
It is not easy to control blood sugar due to diabetes, especially as glomerulus dysfunctions. Proteinuria appears when a hyperglycosemia state lasts a long term, and the filtration function of the kidney decreases. This condition is called “diabetic nephropathy.” Diabetic nephropathy is also one of the Chronic Kidney Diseases (CKD).
If hyperglycemia continues without diabetes treatment, the renal function continues to deteriorate. Eventually, the patient will end up with renal failure, where they lose the ability to produce urine.
Reports show that diabetic nephropathy cases have progressed in recent years, and the number of patients requiring dialysis has been skyrocketing. On the other hand, as diabetic nephropathy progresses, the blood vessels in the glomerulus narrow, the filtering action decreases, and blood pressure rises, leading to developing hypertension. Then, it falls into a vicious cycle of worsening the condition of the kidneys.
Based on the research of “Fucoidan exerts protective effects against diabetic nephropathy related to spontaneous diabetes through the NF-kB signaling pathway in vivo and vitro,” by Yan Wang et al., Diabetic nephropathy (DN) is one of the most critical micro-vessels and is a complication caused by diabetes. Therefore, in this study, researchers investigated Fucoidan’s effect on DNs associated with spontaneous diabetes in Vitro and in Vivo. Goto Kakizaki (GK) rats were free to feed standard rats for 13 weeks with or without Fucoidan and used Wistar rats as controls.
Fucoidan was not cytotoxic to glomerular mesangial cells (GMC) isolated from rat kidneys. Fasting blood glucose levels are measured using a glucose meter. Blood urea nitrogen (BUN) and serum creatinine (Cr) levels are calculated using an automated biochemical analyzer, and urinary protein levels are measured using an ELISA kit.
Collagen IV levels in the renal cortex were measured using an ELISA kit, and the expression levels of transformed growth factors-β1 (TGF-β1) and fibronectin (FN), and nuclear factor-κB (NF-κB) in the renal cortex and GMC. At GMC, it was determined by Western blot analysis. All nuclear translocations, including fasting blood glucose, BUN, serum Cr, urinary protein, collagen IV levels, TGF-β1, FN, and NF-κBp65 expression, were significantly increased in GK rats compared to control Wistar rats. Increased fasting blood glucose, BUN, serum Cr, urinary protein, and collagen IV levels in the renal cortex were reversed in GK rats orally administered Fucoidan.
Oral administration of Fucoidan reduced TGF-β1 and FN expression in the renal cortex and GMC and the nuclear translocation of NF-κBp65 in the GMCs.
In conclusion, data obtained from in vitro and in vivo experiments prove that Fucoidan reduces hyperglycemia and prevents or interferes with the development of DN associated with spontaneous diabetes by weakening the activation of the NF-κB (a pivotal mediator of inflammatory responses) signaling pathway.
