An out of box thinking: the changes of iron-porphyrin during meat processing and gastrointestinal tract and some methods for reducing its potential health hazard.

Iron-porphyrin is a very important substance in organisms, especially in animals. It is not only the source of iron in human body, but is also the catalytic center of many reactions. Previous studies suggested that adequate intake of iron was important for the health of human, especially for children and pregnant women. However, associated diseases caused by iron over-intake and excessive meat consumption suggested its potential harmfulness for human health. During meat processing, Iron-porphyrin will cause the oxidation of proteins and fatty acids. In the gastrointestinal tract, iron-porphyrin can induce the production of malondialdehyde, fats oxidation, and indirectly cause oxidation of amino acids and nitrates etc. Iron-porphyrin enters the intestinal tract and disturbs the balance of intestinal flora. Finally, some common measures for inhibiting its activity are introduced, including the use of chelating agent, antioxidants, competitive inhibitor, etc., as well as give the hypothesis that sodium chloride increases the catalytic activity of iron-porphyrin. The purpose of this review is to present an overview of current knowledge about the changes of iron-porphyrin in the whole technico- and gastrointesto- processing axis and to provide ideas for further research in meat nutrition.

Influence of surface properties on the adhesion of bacteria onto different casings.

Bacteria adhere to the surfaces of sausage casing and form biofilms, which causes food spoilage and quality deterioration. However, bacterial adhesion to the casing surfaces has not received enough attention and has not been extensively studied. In this study, the effect of the physicochemical properties of casing surfaces on bacterial initial adhesion were investigated with Leuconostoc mesenteroides as model bacteria. The adhesion of Leuconostoc mesenteroides onto 5 types of casings were systematically investigated, including animal casings, collagen casings, cellulose casings, fiber casings, and nylon casings, which are the most frequently encountered casings in sausage processing. It was found that the number of viable cells on the casings following the trend as: animal casings > collagen casings > fiber casings > cellulose casings > nylon casings after 4 h of incubation time. This phenomenon might be due to the different physicochemical properties of the different casings. Therefore, physicochemical factors, including zeta potential, hydrophobicity and roughness of casings, zeta potential and hydrophobicity of Leuconostoc mesenteroides, were further characterized. In terms of hydrophobic interactions, the results showed that the number of bacteria attached to the casings did not conform to the trend of hydrophobic interaction. In terms of electrostatic interactions, the results showed that the number of bacteria attached to the casings did not conform to the trend of hydrophobic interaction. The casings with different surface roughnesses in a range of 1.67-20.83 µm, the variation of bacterial adhesion quantity was in good agreement with the variation trend of casing roughness, the result showed that the surface roughness was the key factor dominating the bacterial adhesion rate compared with the surface hydrophobicity and zeta potential. The results give new insights to explore the mechanism of bacterial adhesion on casings and prevent sausage spoilage.

Integrated Network Pharmacology and Cellular Assay to Explore the Mechanisms of Selenized Tripterine Phytosomes (Se@Tri-PTs) Alleviating Podocyte Injury in Diabetic Nephropathy.

AIM: This work aimed to elucidate the mechanisms of Se@Tri-PTs in alleviating podocyte injury via network pharmacology and in vitro cellular assay. BACKGROUND: Selenized tripterine phytosomes (Se@Tri-PTs) have been confirmed to undertake synergistic and sensitized effects on inflammation, which may be curatively promising for diabetic nephropathy (DN). However, the mechanisms of Se@Tri-PTs in alleviating podocyte injury, a major contributor to DN, still remain unclear. OBJECTIVE: The objective of the study was to find out the underlying mechanisms of Se@Tri-PTs in alleviating podocyte injury in diabetic nephropathy. METHODS: The key components and targets of Tripterygium wilfordii (TW) significant for DN as well as the signaling pathways involved have been identified. A high glucose-induced podocyte injury model was established and verified by western blot. The protective concentration of Se@Tri-PTs was screened by CCK-8 assay. Podocytes cultured with high glucose were treated with Se@Tri-PTs under protective levels. The expression of key protective proteins, nephrin and desmin, in podocytes, was assayed by western blot. Further, autophagy- related proteins and factors, like NLRP3, Beclin-1, LC3II/LC3, P62, and SIRT1, were analyzed, which was followed by apoptosis detection. RESULTS: Network pharmacology revealed that several monomeric components of TW, especially Tri, act on DN through multiple targets and pathways, including the NLRP3-mediated inflammatory pathway. Se@Tri-PTs improved the viability of podocytes and alleviated their injury induced by high glucose at 5 µg/L or above. High-glucose induction promoted the expression of NLRP3 in podocytes, while a low concentration of Se@Tri-PTs suppressed the expression. A long-term exposure of high glucose significantly inhibited the autophagic activity of podocytes, as manifested by decreased Beclin-1 level, lower ratio of LC3 II/LC3 I, and up- regulation of P62. This abnormality was efficiently reversed by Se@Tri-PTs. Importantly, the expression of SIRT1 was up-regulated and podocyte apoptosis was reduced. CONCLUSION: Se@Tri-PTs can alleviate podocyte injury associated with DN by modulating NLRP3 expression through the pathway of SIRT1-mediated autophagy.

Effects of Lycium barbarum glycopeptide on renal and testicular injury induced by di(2-ethylhexyl) phthalate.

Di(2-ethylhexyl) phthalate (DEHP) is a common environmental pollutant with renal and reproductive toxicity. Lycium barbarum glycopeptide (LbGp) is the main active component of Lycium barbarum, which can protect the kidney and promote reproduction. Autophagy and apoptosis are the regulatory mechanisms of cell adaptation to external stress. This study investigated whether DEHP and LbGp affect kidney and testis by regulating autophagy and apoptosis. DEHP induced apoptosis in human embryonic kidney-293 (HEK-293) cells and human kidney-2 (HK-2) cells, as well as glomerular enlargement, enhanced renal autophagy and inflammation, decreased testicular germ cells, and enhanced testicular autophagy. LbGp reduced apoptosis in HEK-293 cells and HK-2 cells, reduced glomerular enlargement and renal inflammation, enhanced renal autophagy, increased testicular germ cells, and alleviated testicular autophagy. These results suggested that DEHP induced inflammation to cause kidney injury, mildly enhanced renal autophagy, and also induced excessive autophagy, leading to testicular injury. LbGp reduced inflammation and appropriately enhanced autophagy to alleviate renal injury and also reduced excessive autophagy to alleviate testicular injury. Silent information regulator 1 (SIRT1)/forkhead box O3a (FoxO3a)-mediated autophagy and p38 mitogen-activated protein kinase (p38 MAPK)-mediated inflammation played important roles.