1.
Bioactive peptides from foods: production, function, and application.
Jia, L, Wang, L, Liu, C, Liang, Y, Lin, Q
Food & function. 2021;(16):7108-7125
Abstract
Bioactive peptides are a class of peptides with special physiological functions and have potential applications in human health and disease prevention. Bioactive peptides have gained much research attention because they affect the cardiovascular, endocrine, immune, and nervous systems. Recent research has reported that bioactive peptides are of great value for physiological function regulation, including antioxidation, anti-hypertension, antithrombosis, antibacterial properties, anti-cancer, anti-inflammation, anti-diabetic, anti-obesity, cholesterol-lowering, immunoregulation, mineral binding and opioid activities. The production of food-derived bioactive peptides is mainly through the hydrolysis of digestive enzymes and proteolytic enzymes or microbial fermentation. The purpose of this review is to introduce the production, function, application, challenges, and prospects of food-derived bioactive peptides.
2.
Treatment of FSGS in Children.
Sethna, CB, Gipson, DS
Advances in chronic kidney disease. 2014;(2):194-9
Abstract
Focal segmental glomerulosclerosis (FSGS) is a pathologic condition that represents many disease entities. The goals of therapy are to cure the disease. When this is not possible, the secondary goals are to reduce proteinuria to avoid the complications of nephrotic syndrome and to delay progression of kidney disease. Proteinuria remission is one of the most important independent predictors of kidney survival. Children with FSGS who do not achieve partial or complete remission have a 50% risk of progression to ESRD within 5 years whereas those who enter complete remission have a 5-year kidney survival rate of 90%. Treatment of idiopathic FSGS commonly involves immune-based and nonimmunologic therapy options. This manuscript will review the current state of FSGS therapy for children.
3.
Effects of therapeutic agents on the inflammatory and fibrogenic factors in IgA nephropathy.
Ihm, CG, Jeong, KW, Lee, SH, Lee, TW, Park, JK
Nephrology (Carlton, Vic.). 2007;:S25-6
Abstract
It is desirable in the treatment of IgA nephropathy (IgAN) to prevent the downstream events after the immune response has involved the glomerulus. We and others observed that IgA itself could directly activate mesangial cells to produce monocyte chemotactic peptide-1 (MCP-1), interleukin-6 (IL-6) and transforming growth factor-beta (TGF-beta) and this was suppressed by the treatment with steroid or angiotensin receptor blocker (ARB). It was shown in mesangial cells that the increased expression of TGF-beta and plasminogen activator inhibitor-1 induced by angiotensin II was suppressed by the treatment with ARB, calcium channel blocker (CCB), spironolactone or peroxisome proliferator-activated-receptor-gamma (PPAR-gamma) agonist. It was well known in the patients with IgAN that renal or intraglomerular TGF-beta1 gene expression was increased. Interestingly, treatment with angiotensin-converting enzyme (ACE) inhibitors induced significantly lower renal TGF-beta1 gene expression in patients with IgAN. It was reported in several studies that urinary levels of IL-6, IL-8, MCP-1 or TGF-beta were increased in patients with IgAN. The increase was suppressed by the treatment with steroid, ARB or ACE inhibitor. More effective agents are necessary to ameliorate pathogenetic abnormalities and so to prevent the progression of IgAN.