Safety evaluation and effects of dietary phlorotannins on the growth, health, and intestinal microbiota of Litopenaeus vannamei.

Phlorotannins are phenolic compounds with diverse biological activities, yet their efficacy in aquatic animals currently remains unclear. This investigation scrutinized the influence of phlorotannins on the growth, immunity, antioxidant capacity, and intestinal microbiota in Litopenaeus vannamei, concurrently evaluating the potential adverse effects of phlorotannins on L. vannamei. A base diet without phlorotannins supplementation was used as a control, and 4 groups of diets with different concentrations (0, 0.5, 1.0, 2.0 g kg-1) of phlorotannins were formulated and fed to juvenile shrimp (0.25 ± 0.01 g) for 60 days followed by a 24-h challenge with Vibrio parahaemolyticus with triplicate in each group. Compared with the control, dietary 2.0 g kg-1 phlorotannins significantly improved the growth of the shrimp. The activities of enzymes related to cellular immunity, humoral immunity, and antioxidants, along with a notable upregulation in the expression of related genes, significantly increased. After V. parahaemolyticus challenge, the cumulative survival rates of the shrimp demonstrated a positive correlation with elevated concentrations of phlorotannins. In addition, the abundance of Bacteroidetes and functional genes associated with metabolism increased in phlorotannins supplementation groups. Phlorotannins did not elicit any detrimental effects on the biological macromolecules or histological integrity of the hepatopancreas or intestines. Simultaneously, it led to a significant reduction in malondialdehyde content. All results indicated that phlorotannins at concentrations of 2.0 g kg-1 can be used as safe feed additives to promote the growth, stimulate the immune response, improve the antioxidant capacity and intestinal health of L. vannamei, and an protect shrimp from damage caused by oxidative stress.

The mmu_circ_003062, hsa_circ_0075663/miR-490-3p/CACNA1H axis mediates apoptosis in renal tubular cells in association with endoplasmic reticulum stress following ischemic acute kidney injury.

BACKGROUND: While recent studies have suggested a potential involvement of circRNAs in acute kidney injury (AKI) after ischemia, mmu_circ_003062 role is undetermined. METHODS: The levels of mmu_circ_003062, miR-490-3p, CACNA1H, GRP78, CHOP and hsa_circ_0075663 were detected by Relative qPCR in Boston University mouse proximal tubule (BUMPT) cells, mouse kidneys, and human renal tubular epithelial (HK-2) cells. Moreover, the levels of hsa_circ_0075663 in serum and urine of patients with AKI following cardiopulmonary resuscitation (CPR) were detected by absolute quantitative PCR. Western blot was used to detect the relative expression of the protein. The function and regulatory mechanism of mmu_circ_003062 and hsa_circ_0075663 were investigated through a series of in vitro and in vivo experiments, including bioinformatic prediction, luciferase reporter assays, FISH, FCM, TUNEL staining, and H&E staining. RESULTS: It was found that mmu_circ_003062, hsa_circ_0075663 mediated apoptosis after ischemia/reperfusion (I/R) by interaction with miR-490-3p to enhance CACNA1H expression, thereby leading to the upregulation of endoplasmic reticulum stress (ERS)-relevant proteins GRP78 and CHOP. Ultimately, mmu_circ_003062 downregulation significantly ameliorated ischemic AKI by modulating the miR-490-3p/CACNA1H/GRP78 and CHOP pathway. Furthermore, the plasma and urinary levels of hsa_circ_0075663 in patients with AKI following CPR were significantly higher than non-AKI patients, exhibited a strongly correlation with serum creatinine. CONCLUSION: The involvement of mmu_circ_003062, hsa_circ_0075663/miR-490-3p/CACNA1H/GRP78 and CHOP axis is significant in the development of ischemic AKI. Moreover, hsa_circ_0075663 has potential as an early diagnostic biomarker.

Transcriptome analysis reveals dysfunction of the endoplasmic reticulum protein processing in the sonic muscle of small yellow croaker (Larimichthys polyactis) following noise exposure.

Noise pollution is increasingly prevalent in aquatic ecosystems, causing detrimental effects on growth and behavior of marine fishes. The physiological responses of fish to underwater noise are poorly understood. In this study, we used RNA-sequencing (RNA-seq) to study the transcriptome of the sonic muscle in small yellow croaker (Larimichthys polyactis) after exposure to a 120 dB noise for 30 min. The behavioral experiment revealed that noise exposure resulted in accelerated tail swimming behavior at the beginning of the exposure period, followed by loss of balance at the end of experiment. Transcriptomic analysis found that most highly expressed genes in the sonic muscle, including parvalbumin, slc25a4, and troponin C were related with energy metabolism and locomotor function. Further, a total of 1261 differentially expressed genes (DEGs) were identified, including 284 up-regulated and 977 down-regulated genes in the noise exposure group compared with the control group. Gene ontology (GO) analysis indicated that the most enriched categories of DEGs included protein folding and response to unfolding protein. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis found over-represented pathways including protein processing in the endoplasmic reticulum, chaperones and folding catalysts, as well as arginine and proline metabolism. Specifically, many genes related to fatty acid and collagen metabolism were up-regulated in the noise exposure group. Taken together, our results indicate that exposure to noise stressors alters the swimming behavior of croaker, inducing endoplasmic reticulum stress, disrupting lipid metabolism, and causing collagen degradation in the sonic muscle of L. polyactis.