The impact of mulberry leaf extract at three different levels on reducing the glycemic index of white bread.

In this study, the influences of mulberry leaf extract (MLE) addition on the physicochemical properties including the specific volume, texture and sensory features of white bread (WB) were evaluated by the sensory analysis technology. A double-blind, randomised, repeat-measure design was used to study the impact of MLE addition on the postprandial blood glucose response as well as the satiety index of WB. Results showed that the addition of MLE showed no significant effects on the physicochemical properties of WB except for the slight changes of color and bitterness. The addition of MLE significantly reduced the total blood glucose rise after ingestion of WB over 120 minutes, and reduced the GI value of WB in a dose-effect relationship. When the concentration of MLE reached 1.5 g per 100 g available carbohydrate, the GI value of WB could be reduced from 77 to 43. This study provides important information in terms of the appropriateness of MLE when added to more complex real food, the dose-dependent relationship could supply a reference for the application of MLE.

Effect of Shexiang Baoxin Pill () in Alleviating Early Hypertensive Renal Injury in Rats.

OBJECTIVE: To investigate the effect of Shexiang Baoxin Pill (, SBP) on early hypertensive renal injury in rats and to explore the possible mechanism. METHODS: Twelve-week-old spontaneous hypertensive rats (SHRs) with high-salt diet (dietary containing 8% NaCl) were randomized into the SBP group [40 mg/(kg·d)], losartan potassium group [20 mg/(kg·d)] and saline group by stratified random sampling method, 12 in each group. Blood pressure and urea albumin creatinine ratio were measured. After 10 weeks, the expression levels of serum creatinine (Scr), hypersensitive C-reactive protein (hs-CRP), interleukin (IL)-1 ß, IL-6, tumor necrosis factor α (TNF-α), and transforming growth factor ß (TGF-ß) in serum were assessed. Kidney pathology periodate-schiff staining was performed. Semi-quantitative count of macrophage infiltration was determined by immunochemistry of CD68 staining. Real-time quantitative polymerase chain reaction and Western blot were performed to examine the mRNA and protein expressions of Toll-like receptor 4 (TLR4), nuclear factor κB (NF-κB), monocyte chemokine peptide (MCP-1), inducible nitric oxide synthase (iNOS), and arginase-1 (Arg-1). RESULTS: SBP did not affect the mortality of SHR (P<0.05). SBP significantly reduced the level of elevated blood pressure of SHRs, but the effect was less significantly than that of losartan potassium. SBP decreased urine protein (P<0.01) and the expression levels of IL-1 ß, IL-6, TNF-α, and TGF-ß in serum. The 22-week-old SHRs showed mild proliferation of glomerular endothelial cells, glomerular ischemic lesions, inflammatory cell infiltration in renal tubular interstitium and arteriosclerosis. Both SBP and losartan potassium had alleviated renal pathological change, and significantly reduced the infiltration of macrophage (P<0.05, P<0.01). SBP and losartan potassium decreased the expressions of TLR4, NF-κB, MCP-1, iNOS, and Arg-1. CONCLUSION: SBP significantly modified the early hypertensive renal injury by reducing inflammation, and the effect was similar to losartan potassium.

Atorvastatin improves pathological changes in the aged kidney by upregulating peroxisome proliferator-activated receptor expression and reducing matrix metalloproteinase-9 and transforming growth factor-ß1 levels.

OBJECTIVE: To investigate the effects of atorvastatin (AVT) on renal function and renal pathological changes in the aged rat and explore their possible mechanisms. METHODS: Twenty-month-old, normal female Wistar rats were divided into three groups: group A (n=8) was fed high-dose AVT (10mg/kg/d); group B (n=8) was fed low-dose AVT (1mg/kg/d); and group C (controls, n=8) received the same volume of normal saline; 3-month-old, normal female Wistar rats served as young normal controls (n=8). All rats were sacrificed following a 4-month treatment period. Serum creatinine and blood lipid levels were measured. The glomerular sclerosis index and tubulointerstitial lesions were determined using renal periodic acid-Schiff-stained paraffin sections. The mRNA and protein expressions of matrix metalloproteinases (MMP)-9 and -2, tissue inhibitors of metalloproteinase (TIMP)-1 and -2, transforming growth factor-ß1 (TGF-ß1), and peroxisome proliferator-activated receptors (PPARs) were examined using reverse transcription polymerase chain reactions and Western blots, respectively. RESULTS: Serum lipid (including serum cholesterol and serum triglycerides) levels in aged rats were significantly higher than those in young rats (p<0.05). Compared to the aged control group, high-dose AVT was associated with significantly lower serum total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels in aged rats (p<0.05); low-dose AVT was associated only with lower serum LDL-C levels (p<0.05). Renal morphological changes in aged rats included focal glomerulosclerosis, infiltration of inflammatory cells, and arteriole sclerosis. Improved renal pathology was observed in aged, AVT-treated rats, and included a decreased glomerular sclerosis index and tubulointerstitial lesion score, especially in those receiving high-dose AVT. Additionally, renal artery wall thickening, luminal narrowing, and arteriolosclerosis were significantly less severe in aged rats receiving high-dose AVT. Upregulated expression of MMP-9 and TGF-ß1 was observed in the renal tissue of aged rats. AVT treatment was associated with a reversal of these phenomena and upregulated expression of TIMP-1, PPARα, PPARß, and PPARγ in aged rats. CONCLUSION: AVT improved the renal pathology of aged rats. These effects may have been induced by the lowering of blood lipids, maintaining the MMP/TIMP balance, and downregulating the expression of TGF-ß1. AVT may reduce the levels of MMP-9 and TGF-ß in aged rats by upregulating the expression of PPARs.

[Early renal tubulointerstitial changes and their interventions with Shenkang Injection in diabetic rats].

OBJECTIVE: To explore whether renal tubulointerstitial lesions are early renal pathological changes and its interventions in diabetic rats. METHODS: The type 2 diabetic rat model was induced by a high-sugar and high-fat diet with a low-dose intraperitoneal injection of streptozotocin. And Shenkang Injection (SKI) was used as an intervention drug. A total of 30 Sprague-Dawley rats were divided randomly into diabetic (DM), DM+SKI (DMSK) and normal control (NC) groups. The general status, blood biochemical parameters, microalbuminuria and urinary N-acetyl-D-glueosaminidas (NAG) were recorded. The insulin resistance of diabetic rats was detected with hyperinsulinemic-euglycemic clamp test.Renal pathological changes were evaluated with periodic acid-Schiff (PAS) staining. The expression of Toll-like receptor 4 (TLR4) in kidney tissue and renal interstitial CD68(+) cells was detected with immunohistochemistry. RESULTS: The levels of microalbuminuria, urinary NAG, glomerular volume, renal tubular score, TLR4 expression and renal interstitial CD68(+) cells significantly increased in DM rats with body weight loss and insulin resistance (IOD value of TLR4: 6 289.86 ± 272.45 vs 207.14 ± 22.37; CD68(+) cells: 8.79 ± 0.79 vs.1.23 ± 0.52). All changes in DM rats improved after SKI intervention (P < 0.05). CONCLUSION: Renal tubulointerstitial lesions are early renal damages in type 2 diabetic rats.SKI can attenuate diabetic tubulointerstitial damage and delay the progression of diabetic nephropathy associated with the inhibition of TLR4 expression and inflammation-mediated macrophage infiltration.

Inhibition of calcium(2+)/calmodulin-dependent protein kinase type IV ameliorates experimental nephrotic syndrome.

OBJECTIVE: Evidence has demonstrated that Ca(2+)/calmodulin-dependent protein kinase type IV (CaMKIV) contributes to altered cytokine production by promoting the production of inflammatory cytokines. This study aimed to explore the protective role and underlying mechanisms of CaMKIV inhibition in experimental nephrotic syndrome. METHODS: BALB/c mice received single intravenous injections of adriamycin (10 mg/kg) then were sacrificed at two, four and six weeks. In the second study, treatment with KN-93, a CaMKIV inhibitor, or vehicle administered via intraperitoneal injection was started five days after adriamycin injection. Functional and pathologic parameters, the presence of inflammatory infiltration and the expressions of pro-inflammatory cytokines were assessed. RESULTS: The CaMKIV protein expression levels were upregulated in the mice with adriamycin nephropathy, which was significantly inhibited by KN-93 (p<0.01). As compared with the vehicle-treated controls, KN-93 treatment resulted in marked suppression of proteinuria and serum creatinine at week 6 (p<0.01), but not at two weeks after induction of the disease. KN-93 inhibited glomerulosclerosis and the development of tubulointerstitial lesions. The renal alpha-smooth muscle actin (α-SMA) expression was also significantly suppressed by KN-93 treatment at week 6 (p<0.01). Moreover, KN-93 inhibited the renal monocyte chemoattractant protein-1 (MCP-1) expression, paralleled by a reduction in the interstitial infiltration of macrophages and T-cells (p<0.01). CONCLUSION: Our findings suggest that activation of CaMKIV signaling is involved in the progression of glomerular diseases with a proteinuric state. Our data therefore justify the development of small molecule CaMKIV inhibitors for the treatment of clinical nephrotic syndrome.