Characterization of the physicochemical, thermal and rheological properties of cashew kernel starch.

The study aimed to characterize physicochemical, thermal, and rheological properties of cashew nut starch (CNS) and then compare the obtained results with the properties of potato and corn starches. CNS showed higher gelatinization temperatures (112.29 °C) than those noted for potato and maize starches (78.44-94.65 °C). In addition, CNS had higher peak viscosity (19.03 mPa·s) than high amylose corn starch. The static shear rheological test indicated that the CNS followed a pseudoplastic behavior. In addition, CNS sample showed a thixotropic patter, which was less pronounced than that observed for potato starch, but higher than the value reported for high amylose corn starch. These results demonstrated that the shear resistance of CNS was lower than high amylose corn starch, but higher than potato starch. The storage and loss modulus (G' and G", respectively) of the CNS were higher than those reported for the rest of samples. In this line, elastic properties were predominant in CNS sample. In conclusion, results from this study provided insight into physicochemical and structural properties of cashew nut starch, which could represent a preliminary step for its future application in food processing.

Catechin attenuates TNF-α induced inflammatory response via AMPK-SIRT1 pathway in 3T3-L1 adipocytes.

Chronic inflammation is a fundamental symptom of many diseases. Catechin possesses anti-oxidant and anti-inflammatory properties. However, the mechanism of catechin to prevent inflammation in 3T3-L1 adipocytes caused by TNF-α remains unknown. Therefore, the effects of catechin on the gene expression of cytokines and the activation of cell signals in TNF-α induced 3T3-L1 adipocytes were investigated. The effects of catechin on adipogenesis and cell viability were detected by Oil Red O staining and CCK-8 assay, respectively. The genes expression of cytokines was determined by real-time RT-PCR. The expression of NF-κB, AMPK, FOXO3a and SIRT1 on translation level was determined by western blotting analysis. The results demonstrated that catechin significantly enhanced adipogenesis and cell viability. catechin inhibited the gene expression of pro-inflammatory cytokines including IL-1α, IL-1ß, IL-6, IL-12p35, and inflammatory enzymes including iNOS and COX-2, but enhanced the gene expression of anti-inflammatory cytokines including IL-4 and IL-10. Catechin also inhibited the activation of NF-κB, AMPK, FOXO3a and SIRT1, but increased the phosphorylation level of the above factors. All these results indicated that as a potential therapeutic strategy catechin has the ability of attenuating inflammatory response triggered by TNF-α through signaling cascades involved in inflammation and cytokines.

Hepatocyte growth factor inhibits tubular epithelial­myofibroblast transdifferentiation by suppression of angiotensin II via the JAK2/STAT3 signaling pathway.

Tubular epithelial­myofibroblast transdifferentiation (TEMT) is important in the development of chronic renal failure. The present study investigated whether hepatocyte growth factor (HGF) inhibits TEMT, and whether this function may be associated with the inhibition of angiotensin II (AngII) and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Human HK­2 kidney proximal tubular cells were divided into 4 groups and treated with AngII (1x10­6 M), HGF (8x10­3 M), AngII plus HGF or control conditions, followed by an assessment of apoptosis induction and the expression levels of α­smooth muscle actin (α­SMA), which is a marker of TEMT. as well as the activation level of JAK2, phosphorylated (p)­JAK2, STAT3 and p­STAT3 signaling pathways. In HK­2 cells, α­SMA mRNA and protein expression levels increased following treatment with AngII, however, decreased expression was observed following exposure to HGF. HGF counteracted the AngII­induced increase in the expression of α­SMA in HK­2 cells. Similar expression profiles were observed for the phosphorylated forms of JAK2 and STAT3, indicating the possible involvement of this signaling pathway. The results demonstrated that treatment of cells with AngII was associated with the induction of apoptosis when compared with the control. By contrast, treatment with HGF attenuated AngII­induced apoptosis. The results suggested that HGF may inhibit TEMT by inhibiting AngII through the JAK2/STAT3 signaling pathway in HK­2 cells and HGF may prevent apoptosis induced by AngII. The present study provides a basis for understanding the mechanisms involved in the inhibition of TEMT by HGF, which requires further investigation.

CDX2 enhances HTR-8/SVneo trophoblast cell invasion by altering the expression of matrix metalloproteinases.

BACKGROUND/AIMS: The invasion of trophoblast cells into the maternal uterine decidua is critical for normal placentation, establishment of pregnancy and maintenance of fetal growth in humans. Several growth factors and cytokines have been implicated in trophoblast invasion, but the underlying regulatory mechanisms of invasion are not fully understood. Our earlier studies have found that caudal-related homeobox transcription factor 2 (CDX2) is hypomethylated in human pre-eclampsia placental tissues. However, whether CDX2 is involved in trophoblast invasion was unclear. METHODS AND RESULTS: In this study, we investigated CDX2 function using a human HTR-8/SVneo cell line that overexpressed CDX2. Cell invasion assays demonstrated that CDX2 enhanced trophoblast cell invasiveness. Meanwhile, MTT assays revealed that CDX2 did not affect cell proliferation. Western blot analysis and quantitative real-time PCR demonstrated that the expression level of matrix metalloproteinase-9 (MMP-9) was significantly increased, whereas the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) was markedly suppressed in the CDX2-overexpressing trophoblast cells. The phosphoinositide-3-kinase (PI3K)/Akt signaling pathway is involved in proliferation, migration, metastasis and invasion. Our study showed that inhibition of PI3K/Akt signaling led to decreased expression of CDX2. CONCLUSION: We concluded that CDX2 is likely regulated by the PI3K/Akt signaling pathway during trophoblast cell invasion. Our findings may reveal new insights into the regulatory mechanisms of trophoblast cell invasion and may be an important contributor to the pathogenesis of pregnancy-related diseases.

Pathological changes, TGF-ß1 expression, and the effects of hepatocyte growth factor in 5/6 nephrectomized rats.

Several studies have shown that hepatocyte growth factor (HGF) ameliorates chronic renal failure, but its mechanism of action is unclear. This study was designed to test the delivery of HGF in the PCI-neo vector, using the 5/6 nephrectomized rat as a model for chronic renal failure, and to confirm that this protective function is associated with decreased protein expression of transforming growth factor-beta1 (TGF-ß1). Rats were randomly divided into the following groups: Control (untreated), PCI-neo (vector control), 5/6 nephrectomy, and PCI-neo-HGF. Rats were sacrificed at both the fifth and ninth week after 5/6 nephrectomy. Kidney specimens were used for pathological examination (hematoxylin-eosin staining), and detection of TGF-ß1 protein (Western blot and immunohistochemistry) expression. Blood urea nitrogen, serum creatinine, and 24-h urinary protein excretion (UPE) were increased, renal interstitium was seriously injured, and TGF-ß1 protein expression was elevated in 5/6 nephrectomized rats compared to control rats at either time point. Red blood cell and hemoglobin levels decreased in the ninth week after 5/6 nephrectomy. PCI-neo-HGF expression ameliorated the aforementioned changes and decreased TGF-ß1 expression, not only in the fifth week, but also in the ninth week after surgery. The process of renal injury in the 5/6 nephrectomized rat was consistent with that of chronic renal failure. The increase in TGF-ß1 expression was maintained after 5/6 nephrectomy. HGF relieved chronic renal failure, this protection was associated with down-regulation of TGF-ß1 protein expression, and the protective effects were long-term and stable after 5/6 nephrectomy.

Hepatocyte growth factor-induced amelioration in chronic renal failure is associated with reduced expression of α-smooth muscle actin.

This study aimed to examine whether hepatocyte growth factor (HGF) can improve renal function in 5/6 nephrectomized rats and investigate whether this function is associated with a decrease in α-smooth muscle actin (α-SMA) expression in rat glomerulus mesangial cells and renal interstitium. Rats were randomly divided into the following groups: control, PCI-neo, sham-operation, 5/6 nephrectomy, and low-dose and high-dose PCI-neo-HGF. Rats were killed in the ninth week after 5/6 nephrectomy, and the kidney specimens were subjected to pathological examination by Hematoxylin-Eosin staining and detection of α-SMA expression by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry. The results showed that blood urea nitrogen and serum creatinine levels were increased, renal interstitium was injured, and α-SMA expression was elevated in 5/6 nephrectomized rats compared with that in control. The above changes were ameliorated in the rats injected with PCI-neo-HGF vector. At the molecular level we found that PCI-neo-HGF repressed α-SMA expression in mesangial cells stimulated by lipopolysaccharide. In conclusion, our data suggest that HGF can relieve chronic renal failure, and this protection is associated with the down-regulation of α-SMA expression in mesangial cells and renal interstitium.

Hepatocyte growth factor-induced amelioration in renal interstitial fibrosis is associated with reduced expression of alpha-smooth muscle actin and transforming growth factor-beta1.

Several studies have shown that hepatocyte growth factor (HGF) ameliorates renal interstitial fibrosis, but the mechanism is not fully clear. This study was designed to examine whether HGF can relieve renal interstitial injury in 5/6 nephrectomized rats, and to confirm whether this function was associated with decrease in alpha-smooth muscle actin (alpha-SMA) and transforming growth factor-betal (TGF-beta1) expression. The animals were randomized into 8 groups comprising 6 animals (n = 6) each: control (group I), PCI-neo (group II, 900 microg), sham-operation (group III, not nephrectomy), model or 5/6 nephrectomy group (group IV), lotensin group (an angiotensin converting enzyme inhibitor, group V, 0.6 mg/100 g/day for 5 weeks), low-dose PCI-neo-HGF group (group VI, 690 microg), high-dose PCI-neo-HGF group (group VII, 1380 microg) and lotensin + high-dose PCI-neo-HGF group (group VIII, 0.6 mg/100 g/day for 5 weeks, 1380 microg). The animals were sacrificed in the 5th week after 5/6 nephrectomy. The specimens of kidneys were used for pathological examination (hematoxylin-eosin staining), detection of alpha-SMA and TGF-beta1 mRNA (Reverse transcriptase-polymerase chain reaction) and protein (Western blot and immunohistochemistry) expression. The results showed that in 5/6 nephrectomized rats blood urea nitrogen (BUN), serum creatinine (CRE) and 24 h urinary albumin excretion (UAE) were increased, renal interstitium was injured seriously and alpha-SMA, TGF-beta1 mRNA and protein expression were elevated compared with those of control. The above changes were ameliorated and alpha-SMA and TGF-beta 1 expression was reduced by both PCI-neo-HGF and lotensin. The lotensin + high-dose PCI-neo-HGF group rats exhibited the most significant therapeutic effect both in decreasing the BUN, CRE and 24 h UAE and in relieving renal interstitial injury. In conclusion, the study demonstrated that HGF can relieve renal interstitial injury and this protection was associated with down-regulation of a-SMA and TGF-beta 1 expressions.