Jiun-Rong Chen

Identification of Antihypertensive Peptides from Peptic Digest of Two Microalgae, Chlorella vulgaris and Spirulina platensis

Abstract: The peptidic fractions that inhibited angiotensin I–converting enzyme (ACE) were separated from the peptic digests of 2 microalgae, Chlorella vulgaris and Spirulina platensis, by ion exchange chromatography and gel filtration. Oral administration of peptidic fractions into spontaneously hypertensive rats at 200 mg/kg of body weight resulted in marked antihypertensive effects. Further separation of the peptidic fractions by ODS high-performance liquid chromatography furnished the following active peptides: Ile-Val-Val-Glu (inhibitory against ACE with an IC50 of 315.3 μM), Ala-Phe-Leu (63.8 μM), Phe-Ala-Leu (26.3 μM), Ala-Glu-Leu (57.1 μM), and Val-Val-Pro-Pro-Ala (79.5 μM) from C. vulgaris; Ile-Ala-Glu (34.7 μM), Phe-Ala-Leu, Ala-Glu-Leu, Ile-Ala-Pro-Gly (11.4 μM), and Val-Ala-Phe (35.8 μM) from S. platensis.

Soy protein retards the progression of non-alcoholic steatohepatitis via improvement of insulin resistance and steatosis

OBJECTIVE Non-alcoholic steatohepatitis (NASH) is a common cause of liver disease, and it may progress to fibrosis or cirrhosis. The aim of this study was to investigate the effects of soy protein on hepatic steatosis and insulin resistance in NASH. METHODS Forty male Sprague-Dawley rats were fed a high-fat diet for 4 wk to induce NASH and then were allocated to one of four diets: a NASH-inducing diet, a standard diet, a NASH-inducing diet plus soy protein, and a standard diet plus soy protein. RESULTS After the 10-wk experimental period, the results showed that soy protein significantly lowered plasma cholesterol concentrations and body fat accumulation. Soy protein intake also decreased the hepatic lipid depots of triacylglycerols and cholesterol and decreased the concentrations of lipid peroxides. In an analysis of antioxidative status, rats fed the soy protein diet showed improved antioxidative potential due to increases in superoxide dismutase and catalase activities and a decrease in the protein expression of cytochrome P450 2E1. CONCLUSION Soy protein may improve the liver function in patients with NASH by lowering lipid levels in the blood and liver, increasing the antioxidative capacity, and improving insulin resistance.

Effects of glutamine administration on inflammatory responses in chronic ethanol-fed rats

The purpose of this study was to investigate the effects of glutamine supplementation on inflammatory responses in chronic ethanol-fed rats. Male Wistar rats weighing about 160 g were divided into five groups. Two groups were fed a normal liquid diet and three groups were fed a glutamine-containing liquid diet. After 1 week, one of the normal liquid diet groups was fed an ethanol-containing liquid diet (CE), and the other group served as the control (CC) group. At the same time, one of the glutamine-containing liquid diet groups was continually fed the same diet (GCG), but the other two groups were fed ethanol-containing diet supplemented with glutamine (GEG) or without glutamine (GE). The following items were analyzed: (1) liver function, (2) cytokine contents, and (3) hepatic oxidative stress. The activities of aspartate transaminase (AST) and alanine transaminase (ALT) and levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the CE group had significantly increased. In addition, hepatic cytochrome P450 2E1 (CYP2E1) expression had significantly increased in the CE, GE and GEG groups. However, the activities of AST and ALT and levels of TNF-α and IL-1β in the GE group were significantly lower than those of the CE group. The results suggest that the plasma inflammatory responses of rats fed an ethanol-containing liquid diet for 7 weeks significantly increased. However, pretreatment with glutamine improved the plasma inflammatory responses induced by ethanol.

Long-term administration of advanced glycation end-product stimulates the activation of NLRP3 inflammasome and sparking the development of renal injury

The accumulation of advanced glycation end-products (AGEs) and the enhanced interaction of AGE with their cellular receptor (RAGE) have been implicated in the progression of chronic kidney disease. The purpose of this study was to examine whether the AGE/RAGE-induced nephrotoxic effects are associated with inflammasome activation and endothelial dysfunction. Chronic renal injury was examined in BALB/c mice by the long-term administration of carbonyl-AGE for 16 weeks. Endothelial dysfunction was detected by measuring the number of circulating endothelial progenitor cells (EPCs) and the levels of nitric oxide synthase (eNOS) and nitric oxide (NO) in kidneys. Results showed that administration of methylglyoxal-bovine serum albumin (MG-BSA) AGE accelerated renal MG, carboxyethyl lysine, carboxymethyl lysine and malondialdehyde formation and, in parallel, the levels of serum creatinine and blood urea nitrogen (BUN) were significantly increased. Expression of RAGE and NLRP3 inflammasome-related proteins (TXNIP, NLRP3, procaspase-1 and caspase-1) and IL (interleukin)-1β secretion were upregulated, whereas the levels of EPCs, eNOS and NO were lower in MG-BSA-treated mice. This induction by MG-BSA was significantly inhibited by RAGE antagonist. Our results firstly reveal a possible mechanism of AGE-mediated renal dysfunction upon NLRP3 inflammasome activation. Therapeutic blockade of RAGE may ameliorate renal and endothelial functions in subjects under high AGE burden.