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In order to reduce the amount of added sodium in myofibrillar protein (MP) gel, the effects of partial substitution of different chloride salts (CaCl2, MgCl2, and KCl) for NaCl on the gel strength, microstructure, water-holding capacity and rheological properties of MP gel were studied. The underlying mechanism of action of sodium substitutes was elucidated by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and intrinsic fluorescence spectroscopy as well as measuring surface hydrophobicity and sulfhydryl content. The results showed that KCl was the best substitute for NaCl, followed by CaCl2, and MgCl2 was least effective in replacing NaCl. The gel strength of the KCl substitution groups (0.5% KCl + 2.5% NaCl, 1.5% KCl + 1.5% NaCl, and 1.0% KCl + 2.0% NaCl; m/m) was better than that of the control group (3% NaCl), while no significant difference in water-holding capacity was found between the two groups (P > 0.05). The gel strength of the 1.5% CaCl2 + 1.5% NaCl group decreased significantly (P < 0.05), and the water-holding capacity decreased first and then increased. The gel strength significantly decreased (P < 0.05) and the water-holding capacity increased in the MgCl2 substitution groups. In terms of rheological properties, the storage modulus (G’) of the KCl substitution groups was significantly higher than that of the control group. Substitution of CaCl2 and MgCl2 increased the surface hydrophobicity of MP and decreased the sulfhydryl content. Substitution of CaCl2, MgCl2, and KCl resulted in a blue shift in intrinsic fluorescence spectra. At low substitution levels (0.5%), the microstructure of MP gel showed no significant difference from that of the control group. The above results indicate that CaCl2, MgCl2 and KCl can be used to partially substitute NaCl in surimi gel products.

The influence of epigallocatechin gallate (EGCG) on the physicochemical–rheological properties of silver carp surimi gel was investigated. The gel strength, texture, water-holding capacity (WHC), dynamic distribution of water, and rheological properties of surimi gels added with different levels (0, 0.02, 0.04, 0.06, 0.08, and 0.1%) of EGCG were measured. The results showed that with the increase of EGCG content, the gel strength, hardness, WHC, and immobilized water contents of surimi gels showed a trend of first increasing and then decreasing, and EGCG 0.02% and EGCG 0.04% showed better gel performance as compared with the control. EGCG 0.02% had the highest gel strength (406.62 g·cm), hardness (356.67 g), WHC (64.37%), and immobilized water contents (98.958%). The gel performance decreased significantly when the amounts of EGCG were higher than 0.06%. The viscosity, G′, and G″ of the rheological properties also showed the same trends. The chemical interaction of surimi gels, secondary structure of myofibrillar protein (MP), and molecular docking results of EGCG and silver carp myosin showed that EGCG mainly affected the structure and aggregation behavior of silver carp myosin through non-covalent interactions such as those of hydrogen bonds, hydrophobic interactions, and electrostatic interactions. The microstructures of EGCG 0.02% and EGCG 0.04% were compact and homogeneous, and had better gel formation ability. The lower concentrations of EGCG formed a large number of chemical interactions such as those of disulfide bonds and hydrophobic interactions inside the surimi gels by proper cross-linking with MP, and also increased the ordered β-sheet structure of MP, which facilitated the formation of the compact three-dimensional network gel. [ABSTRACT FROM AUTHOR]

Glioma is a malignant primary brain tumor that occurs in the central nervous system and has threatened the well-being of millions of patients. It is well acknowledged that long non-coding RNA (lncRNA) SNHG3 participates in the regulation of proliferation, inflation, differentiation, and metastasis in many cancers. However, the regulatory effect of SNHG3 on glioma progression is still controversial. The expression of SNHG3 and HDGF was upregulated, whereas miR-384 was downregulated in glioma tissues, compared with the normal tissues. Interestingly, high SNHG3 contributed to low survival rate while low SNHG3 showed the opposite result. Moreover, SNHG3 or HDGF knockdown significantly suppressed proliferation, migration, and invasion and induced apoptosis in glioma. Meanwhile, restoration of HDGF abrogated the inhibition of SNHG3 silencing on glioma cell progression. Besides, miR-384 inhibitor attenuated SNHG3 silencing induced inhibition on HDGF mRNA and protein expression in A172 and SHG44 cells. LncRNA SNHG3 promotes cell proliferation, migration, and invasion in glioma by enhancing HDGF expression via miR-384 sponging, representing the promising targets for the development of novel therapeutic strategies.