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To better understand the ecological effects of mariculture, the diversity distribution, determinant and interaction of microeukaryote communities from fish cage and suspended shellfish farming were investigated in three bays of South China Coast. Our alpha and beta diversity analyses showed that the difference of the microeukaryote community between fish and shellfish farming was more significant at local than regional scale, and microeukaryotes respond more to spatial effect than mariculture effect at regional scale. Mantel test, variation partitioning analysis and co-occurrence network analysis revealed that the environmental factors especially chemical and biotic factors contributed more to community assembly in fish than shellfish farming. Based on the comparisons of community composition and determinant between fish and shellfish farming, the effect mechanisms of the two farming types on microeukaryote community were proposed. Fish farming brings significant environmental variation and thus has strong bottom-up impacts on microeukaryotes, while shellfish farming exerts a grazing pressure on microeukaryotes by filter-feeding and has top-down control to them. Furthermore, the network stability analyses revealed weaker community stability in fish than shellfish farming, suggesting that the microeukaryote community was more sensitive to environmental change deduced by fish than shellfish farming. Overall, this study revealed the different influencing mechanisms of fish and shellfish mariculture on microeukaryotes, which will improve the understanding of the ecological effects of mariculture and provide guidance for the management of mariculture under future environmental pressures. [Display omitted] • Effects of mariculture on microeukaryotic community was more significant at local than regional scale. • Chemical and biotic factors contributed more to community assembly in fish than shellfish farming. • Fish farming had strong bottom-up impacts on microeukaryotic community; Shellfish farming exerted top-down control to them. • Microeukaryote community was more sensitive to environmental change deduced by fish than shellfish farming. • Management practices and ecological remediation should be carried out in principle of adaptation to mariculture types. [ABSTRACT FROM AUTHOR]

The role of bioactive peptides in diabetes management has attracted extensive attention. In this study, the 1–3 kDa fraction of rice bran peptides (RBPs) was obtained by the hydrolysis of alkaline and dispase, and the following ultrafiltration demonstrated excellent α-glucosidase inhibition activity with an IC 50 value of 1.17 ± 0.08 mg/mL and exhibited postprandial hypoglycemic activity in vivo. Enzymatic kinetics studies revealed that RBPs (1–3 kDa) inhibited α-glucosidase via competitive inhibition. Thirty-two peptides were characterized from RBPs (1–3 kDa) by LC-MS/MS. Virtual screening was applied to screening the new potential α-glucosidase inhibitor, and NVEKKDPTGA (NA-10) with a binding energy of −10.24 kcal/mol to α-glucosidase was selected as the most promising peptide. Molecular docking reflected that Ala at the C-terminal and KK amino acid cluster play a key role in forming hydrogen bonds with the catalytic site of α-glucosidase, which might be critical for the α-glucosidase inhibitory effect. This study proved that RBPs could be a promising bio-factor food ingredient for diabetes prevention. 1–3 kDa fraction of rice bran peptides showed the best α-glucosidase inhibition activity with an IC 50 value of 1.17 ± 0.08 mg/mL and exhibited hypoglycemic effect on maltose tolerance test in mice. Molecular docking results revealed that Ala at C-terminal and KK amino acid cluster in rice bran peptides play a key role in its α-glucosidase inhibition activity. Rice bran peptides would be a promising factor to inhibit α-glucosidase. [Display omitted] • 1–3 kDa (1.17 ± 0.08 mg/mL) fraction showed the best α-glucosidase inhibition activity. • Rice bran peptides exhibited hypoglycemic effect on maltose tolerance test in mice. • Ala at C-terminal and KK amino acid cluster play a key role. [ABSTRACT FROM AUTHOR]

Collagen I is a major component of extracellular matrix in human skin, and is also widely used in a variety of skin-care products. In this study, we investigated the modulatory roles of collagen I on human immortalized keratinocytes HaCaT, especially when cells were irradiated with UVB. Interestingly, the cells grown on plates coated by molecular collagen I, but not fibrillar collagen I, acquired certain resistance against UVB damages, as shown by increased survival and reduced apoptosis. The accumulation of dysfunctional mitochondria in UVB-treated cells was attenuated by molecular collagen I-coating. Interestingly, molecular collagen I rescued the loss of mitochondrial biogenesis in cells treated with UVB. Loss of PINK1/parkin-mediated mitophagy was dominant for the accumulation of dysfunctional mitochondria after UVB irradiation. Of note, cells cultured on molecular collagen I-precoated plates exhibited reserved mitophagy after UVB irradiation, as reflected by the enhanced protein level of PINK1/parkin, increased mitochondrial ubiquitin and the co-localization of lysosomes and mitochondria. Moreover, in UVB-treated cells, inhibiting mitophagy by Cyclosporin A, or by silencing PINK1 or parkin, disturbed the resolution of mitochondrial stress and reduced the protective effect of molecular collagen I, indicating that mitophagy is pivotal for the protection of collagen I against UVB damage in keratinocytes HaCaT. Collectively, this study reveals an unexpected protective role of collagen I, which facilitates mitophagy to rescue cells under UVB irradiation, providing a new direction for clinical application of collagen products. [Display omitted] • Precoating culture plates with collagen I alleviates UVB-induced HaCaT cell apoptosis. • Collagen I inhibits the accumulation of damaged mitochondria in UVB-treated cells. • Arrest of mitophagy accelerates UVB damage by accumulating damaged mitochondria. • UVB protection caused by collagen I depends on rescuing mitophagy. [ABSTRACT FROM AUTHOR]