Sea buckthorn oil regulates primary myoblasts proliferation and differentiation in vitro.

Skeletal muscle is the main edible part of meat products, and its development directly affects the yield and palatability of meat. Sea buckthorn oil (SBO) contains plenty of bioactive substances and has been recognized as a potential functional food product. The study aimed to explore the effects and possible mechanisms of SBO on sheep primary myoblast proliferation and myogenic differentiation. The results implied that SBO exhibited a pro-proliferative effect on primary myoblasts, along with up-regulated proliferating cell nuclear antigen (PCNA) and Cyclin D1/cyclin-dependent kinase 4 (CDK4) abundances. And, SBO promoted myotube formation by increasing the expression of myogenin. Meanwhile, we found that SBO inhibited the expression of miRNA-292a. Moreover, the regulatory effect of SBO on myogenic differentiation of myoblasts was attenuated by miRNA-292a mimics. Of note, SBO activated protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway and augmented glucose uptake and glucose transporter 4 (GLUT4) content, which might be attributed to AMP-activated protein kinase (AMPK) activation. Additionally, the results were shown that SBO increased the abundance of antioxidative enzymes, including glutathione peroxidase 4 (Gpx4) and catalase. In summary, these data suggested that SBO regulated the proliferation and myogenic differentiation of sheep primary myoblasts in vitro, which might potentiate the application of SBO in muscle growth.

Intramuscular vitamin A injection in newborn lambs enhances antioxidant capacity and improves meat quality.

Introduction: Vitamin A (VA) and its metabolite, retinoic acid (RA) possess several biological functions. This report investigated whether neonatal intramuscular VA injection affected antioxidative activity and meat quality in longissimus dorsi (LD) muscle of lambs. Methods: Lambs were injected with 0 (control) or 7,500 IU VA palmitate into the biceps femoris muscle on day 2 after birth. At 3, 12, and 32 weeks of age, blood samples were collected in the jugular vein for serum levels of RA and muscle samples were collected in the biceps femoris for analysis of relative mRNA expression of enzyme contributors to retinoid metabolism. All animals were harvested at 32 weeks of age and muscle samples were collected to explore the role of VA on the meat quality and antioxidant capacity of lambs. Results and discussion: Our results indicated that VA increased the redness, crude protein, and crude fat (p < 0.05), without affecting moisture, ash, and amino acid composition in LD muscle (p > 0.05). In addition, VA increased catalase (CAT) activity and decreased malondialdehyde (MDA) levels in LD muscle (p < 0.05). Meanwhile, greater levels of CAT and NRF2 mRNA and protein contents with VA treatment were observed in LD muscle (p < 0.05), partly explained by the increased level of RA (p < 0.05). Collectively, our findings indicated that VA injection at birth could improve lamb meat quality by elevating the redness, crude protein, crude fat, and antioxidative capacity in LD muscle of lambs.

Circ-PRKDC Facilitates the Progression of Colorectal Cancer Through miR-198/DDR1 Regulatory Axis.

BACKGROUND: Circular RNAs (circRNAs) play a crucial role in a variety of cancers, including colorectal cancer (CRC). This study aimed to explore the role of hsa_circ_0136666 (circ-PRKDC) in CRC and its potential mechanism. METHODS: The levels of circ-PRKDC, miR-198 and discoidin domain receptor 1 (DDR1) were measured using quantitative real-time polymerase chain reaction or Western blot. Cell viability was detected using cell counting kit-8 (CCK-8) assay. Cell apoptosis and cycle were evaluated via flow cytometry. Cell migration and invasion were examined using transwell assay. CyclinD1 protein level was determined via Western blot. The interaction among circ-PRKDC, miR-198 and DDR1 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Xenograft assay was performed to analyze tumor growth in vivo. RESULTS: Circ-PRKDC and DDR1 levels were increased, and miR-198 level was decreased in CRC tissues and cells. Circ-PRKDC depletion inhibited proliferation, migration and invasion, and expedited apoptosis and cell cycle arrest in SW480 and HCT116 cells. Silence of circ-PRKDC impeded CRC progression by sponging miR-198. Overexpression of miR-198 hindered CRC development via targeting DDR1. Moreover, circ-PRKDC silencing suppressed tumor growth in vivo. CONCLUSION: Knockdown of circ-PRKDC inhibited CRC progression via modulating miR-198/DDR1 pathway.