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Being an important crop, soybean is widely used in the world and plays a vital role in human and animal nutrition. However, it contains several antinutritional factors (ANFs) including soybean agglutinin, soybean protease inhibitors, soybean allergenic proteins, etc., that may result in poor food utilization, decreased growth performance, and even disease. Among these ANFs, soybean allergenic proteins can lead to allergic reactions in human and animals, which has become a public problem all over the world, but our knowledge on it is still inadequate. This paper aims to provide an update on the characteristics, detection or exploration methods, and in vivo research models of soybean allergenic proteins; especially glycinin and β-conglycinin are deeply discussed. Through this review, we may have a better understanding on the advances of research on these two soybean allergenic proteins. Besides, the ingredient processing used to reduce the allergenicity of soybean is also reviewed. [ABSTRACT FROM AUTHOR]

Backgrounds: Autophagy is an important process in the pathogenesis of diabetes and plays a critical role in maintaining cellular homeostasis. However, the autophagic response and its mechanism in diabetic vascular endothelium remain unclear. Methods and Results: We studied high-glucose-induced renin-angiotensin system (RAS)-mitochondrial damage and its effect on endothelial cells. With regard to therapeutics, we investigated the beneficial effect of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs) against high-glucose-induced endothelial responses. High glucose activated RAS, enhanced mitochondrial damage and increased senescence, apoptosis and autophagic-responses in endothelial cells, and these effects were mimicked by using angiotensin II (Ang). The use of an ACEI or ARB, however, inhibited the negative effects of high glucose. Direct mitochondrial injury caused by carbonyl cyanide 3-chlorophenylhydrazone (CCCP) resulted in similar negative effects of high glucose or Ang and abrogated the protective effects of an ACEI or ARB. Additionally, by impairing autophagy, high-glucose-induced senescence and apoptosis were accelerated and the ACEI- or ARB-mediated beneficial effects were abolished. Furthermore, increases in FragEL™ DNA Fragmentation (TUNEL)-positive cells, β-galactosidase activation and the expression of autophagic biomarkers were revealed in diabetic patients and rats, and the treatment with an ACEI or ARB decreased these responses. Conclusions: These data suggest that autophagy protects against senescence and apoptosis via RAS-mitochondria in high-glucose-induced endothelial cells. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: The effects of n-3 highly unsaturated fatty acid (n-3 HUFA) content in broodstock diets on the quality and fatty acid composition of eggs and larvae were investigated in Plectorhynchus cinctus. Broodstocks were fed a natural diet (trash fish) and four formulated diets with similar proximate compositions but different levels of n-3 HUFA (1.12, 2.40, 3.70 or 5.85%) through their reproductive cycle. Compared with the natural diet-fed group, the egg production per kg of females, percentage of buoyant eggs, survival and length of larvae at 3 days post hatching were similar in fish fed 2.40% and 3.70% n-3 HUFA diets, but markedly decreased in the groups fed 1.12 and 5.85% n-3 HUFA diets. The content of most fatty acids and fatty acid class in eggs and larvae was directly influenced by dietary n-3 HUFA levels and exhibited parallel change pattern with the respective dietary levels. The results showed that either deficient or excess level of dietary n-3 HUFA had a negative effect on egg and larval quality, good spawning performance was obtained when the dietary n-3 HUFA content was 2.40 and 3.70%, or the n-3 HUFA level took 12.17 and 18.63% of the total fatty acids. Dietary n-3 HUFA content may affect egg and larval quality by influencing their fatty acid composition. [Copyright &y& Elsevier]

Abstract: Δ6-Desaturase (linoleoyl-CoA desaturase, EC 1.14.19.3) is the rate-limiting enzyme in the biosynthetic pathway of highly unsaturated fatty acid (HUFA). In this report, a Δ6 desaturase-like cDNA was cloned, and the relation of HUFA biosynthetic activity in liver with ambient salinity as well as dietary fatty acids was investigated in the euryhaline teleost Siganus canaliculatus. After the juveniles were fed four formulated diets (D1–D4) with different essential fatty acid composition (D1 with 23.49% HUFA, D2–D4 were HUFA-free, linoleic and α-linolenic acids account for 21.1% and 0.38%, 13.99% and 11.64%, 18.31% and 5.82% of the total fatty acids, respectively) for nine weeks, the growth performance showed no difference among groups in brackish water (10 ppt) or seawater (32 ppt) (P >0.05). Comparing liver fatty acids with fish fed D1, the content of arachidonic acid in fish fed D2 or D4 was significantly higher in 10 ppt (P <0.05), but showed no difference in 32 ppt; the contents of eicosapentaenoic (EPA), docosapentaenoic (DPA) and docosahexaenoic (DHA) acids in 10 ppt, as well as EPA in 32 ppt in fish fed D3 showed no difference, whereas those of DPA and DHA were significantly lower in 32 ppt (P <0.05). These data suggest that S. canaliculatus may convert linoleic and α-linolenic acids into HUFA and such a capacity was stronger in low salinity than that in high salinity. Consistent with this, the liver levels of Δ6 desaturase mRNA in fish fed D2–D4 were generally higher than in fish fed D1 in both salinities, and the total expression level in 10 ppt was about 1.56 times of that in 32 ppt, suggesting that transcriptional control of Δ6 desaturase is involved in such a HUFA biosynthesis. To our knowledge, this is the first report showing the relation of HUFA biosynthetic activity with ambient salinity in a euryhaline fish. [Copyright &y& Elsevier]

The exact mechanism associated with inflammation and atrial fibrillation (AF) remains unknown. The aim of the present study was to investigate the roles of connexin 43 (Cx43) and a1‑adrenergic receptor (α1‑AR) activation in the pathogenesis of system inflammation‑induced AF. A canine model of chronic low‑grade system inflammation was established by administrating a low dose of lipopolysaccharide (LPS; 0.1 µg/kg) for 2 weeks. Programmed stimulation was applied on the right atrial appendage to determine the effective refractory periods (ERP) and the window of vulnerability (WOV). Tumor necrosis factor α (TNF‑α) and interleukin 6 (IL‑6) levels in plasma and atrial tissue were measured by ELISA. Cx43, Toll‑like receptor 4 (TLR4) and nuclear factor κB (NF‑κB) proteins were analyzed using western blotting or immunohistochemistry. Administration of LPS for 2 weeks increased the concentration of TNF‑α and IL‑6 in the plasma and right atrium. ERP was markedly shortened and cumulative WOV was significantly widened in the LPS group. Following treatment with LPS, the amount of Cx43 protein in the area of intercalated disk increased. In addition, a high‑density of Cx43 in the lateral connection was identified. LPS also induced the activation of NF‑κB in the canine atrium. Administration with the α1‑AR blocker doxazosin prevented the production of LPS‑induced inflammatory cytokine and reversed the enhanced vulnerability to atrial fibrillation. Doxazosin inhibited the LPS‑induced increase in Cx43 protein and heterogeneous distribution, and prevented the activation of NF‑κB. These results indicated that chronic low‑grade system inflammation may increase the inducibility of AF in a canine model. The underlying mechanism may be involved in the LPS‑induced activation of NF‑κB, and the increase in Cx43 expression and lateral distribution via an α1-AR-dependent pathway.

Lycopene (Ly), the most common type of antioxidant in the majority of diet types, provides tolerance to ischemia/reperfusion injury. However, the underlying mechanism of the protective effects observed following Ly administration remains poorly investigated. The aim of the current study was to investigate whether Ly prevents damage to hypoxia/reoxygenation (HR)‑induced H9C2 myocardioblasts in an autophagy‑dependent manner. The levels of autophagic markers were detected using western blotting, the level of apoptosis was detected using western blotting and flow cytometry. The activation of autophagy was impaired via knockdown of the expression of 'microtubule‑associated protein 1‑light chain 3β (MAP1LC3B)' and 'Beclin 1'. After 16 h hypoxia, followed by 2 h reoxygenation, the expression levels of the microtubule‑associated protein 1A/1B‑light chain 3 (LC3) and Βeclin 1 autophagic biomarkers, and cell viability were reduced, whereas the percentage of apoptotic cells, and the expression levels of the Bax/B‑cell lymphoma 2 (Bcl‑2) and active caspase‑3 apoptotic biomarkers were increased. Pre‑incubation of the cells with different Ly concentrations reversed the HR‑induced inhibition of autophagy and cell viability, and the HR‑induced elevation in apoptotic levels. The induction of autophagy was accompanied by reduced apoptosis, and decreased expression levels of Bax/Bcl‑2 and active caspase‑3. In addition, the impairment of autophagy by silencing the expression of MAP1LC3B and Beclin 1 accelerated HR‑induced H9C2 cell apoptosis and the Ly‑mediated protective effects disappeared. Furthermore, Bax/Bcl‑2 and active caspase‑3 expression levels were increased. Moreover, Ly‑induced autophagy was associated with increased adenosine monophosphate kinase (AMPK) phosphorylation. Suppressed AMPK phosphorylation using compound C terminates Ly‑mediated cytoprotective effects. Ly treatment improves cell viability and reduces apoptosis as a result of the activation of the adaptive autophagic response on HR‑induced H9C2 myocardioblasts. AMPK phosphorylation may be involved in the progression.

Delta(6)-Desaturase (linoleoyl-CoA desaturase, EC 1.14.19.3) is the rate-limiting enzyme in the biosynthetic pathway of highly unsaturated fatty acid (HUFA). In this report, a Delta6 desaturase-like cDNA was cloned, and the relation of HUFA biosynthetic activity in liver with ambient salinity as well as dietary fatty acids was investigated in the euryhaline teleost Siganus canaliculatus. After the juveniles were fed four formulated diets (D1-D4) with different essential fatty acid composition (D1 with 23.49% HUFA, D2-D4 were HUFA-free, linoleic and alpha-linolenic acids account for 21.1% and 0.38%, 13.99% and 11.64%, 18.31% and 5.82% of the total fatty acids, respectively) for nine weeks, the growth performance showed no difference among groups in brackish water (10 ppt) or seawater (32 ppt) (P>0.05). Comparing liver fatty acids with fish fed D1, the content of arachidonic acid in fish fed D2 or D4 was significantly higher in 10 ppt (P<0.05), but showed no difference in 32 ppt; the contents of eicosapentaenoic (EPA), docosapentaenoic (DPA) and docosahexaenoic (DHA) acids in 10 ppt, as well as EPA in 32 ppt in fish fed D3 showed no difference, whereas those of DPA and DHA were significantly lower in 32 ppt (P<0.05). These data suggest that S. canaliculatus may convert linoleic and alpha-linolenic acids into HUFA and such a capacity was stronger in low salinity than that in high salinity. Consistent with this, the liver levels of Delta6 desaturase mRNA in fish fed D2-D4 were generally higher than in fish fed D1 in both salinities, and the total expression level in 10 ppt was about 1.56 times of that in 32 ppt, suggesting that transcriptional control of Delta6 desaturase is involved in such a HUFA biosynthesis. To our knowledge, this is the first report showing the relation of HUFA biosynthetic activity with ambient salinity in a euryhaline fish.