In plants, the role of anthocyanins trafficking in response to high temperature has been rarely studied, and therefore poorly understood. Red-fleshed kiwifruit has stimulated the world kiwifruit industry owing to its appealing color. However, fruit in warmer climates have been found to have poor flesh coloration, and the factors responsible for this response remain elusive. Partial correlation and regression analysis confirmed that accumulative temperatures above 25 °C (T25) was one of the dominant factors inhibiting anthocyanin accumulation in red-fleshed Actinidia chinensis, 'Hongyang'. Expression of structural genes, AcMRP and AcMYB1 in inner pericarp sampled from the two high altitudes (low temperature area), was notably higher than the low altitude (high temperature area) during fruit coloration. AcMYB1 and structural genes coordinate expression supported the MYB-bHLH (basic helix-loop-helix)-WD40 regulatory complex mediated downregulation of anthocyanin biosynthesis induced by high temperatures in kiwifruit. Moreover, cytological observations using the light and transmission electronic microscopy showed that there were a series of anthocyanic vacuolar inclusion (AVI)-like structures involved in their vacuolization process and dissolution of the pigmented bodies inside cells of fruit inner pericarp. Anthocyanin transport was inhibited by high temperature via retardation of vacuolization or reduction in AIV-like structure formation. Our findings strongly suggested that complex multimechanisms influenced the effects of high temperature on red-fleshed kiwifruit coloration.

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Non-alcoholic fatty liver disease (NAFLD) is caused by fat accumulation and is associated with abnormal cholesterol metabolism. Previous work indicates that polysaccharides from alga Enteromorpha prolifera improve glucose metabolism and lower cholesterol in diabetic rats. Thus, we studied the possible protective effects of E. prolifera polysaccharides (EP) in the development of NAFLD and underlying mechanisms. EP (200 mg kg) significantly reduced the liver weight and significantly lowered hepatic HMG-CoA reductase (HMGCR) mRNA protein expression. EP suppressed sterol regulatory element binding protein-2, which is a key transcription factor in cholesterol metabolism and regulates the expression of HMGCR. Therefore, EP may be a functional food that can prevent NAFLD.

Enteromorpha prolifera is an edible alga and previous studies have indicated that E. prolifera polysaccharide (EP) attenuates non-alcoholic fatty liver disease (NAFLD) in high-fat diet rats. Hydrogen sulfide (H2S) has recently been found to exert many physiological effects. The purpose of this study was to evaluate whether EP prevents NAFLD via regulation of H2S production. EP was orally administered to high-fat diet rats for 5 weeks. Treatment with EP (200 mg per kg body weight per d) significantly increased the serum H2S level and reduced the serum triglyceride level (p < 0.05) in rats fed a high-fat diet. These effects were similar to those observed with NaHS, a H2S donor. Real-time PCR and western blotting analysis revealed that EP significantly upregulated hepatic mRNA and protein expression of cystathionine-β-synthase, which is the enzyme responsible for H2S production. These results indicate that EP decreases the serum TG level by increasing H2S production, suggesting that EP may be beneficial for the treatment of NAFLD and may reduce the risk of cardiovascular disease.

Background: Non-alcoholic fatty liver disease (NAFLD) is a burgeoning health problem but no drug has been approved for its treatment. Animal experiments and clinical trials have demonstrated the beneficial of saffron on NAFLD. However, the bioactive ingredients and therapeutic targets of saffron on NAFLD are unclear.Purpose: This study aimed to identify the bioactive ingredients of saffron responsible for its effects on NAFLD and explore its therapy targets through network pharmacology combined with experimental tests.Methods: Various network databases were searched to identify bioactive ingredients of saffron and identify NAFLD-related targets. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were conducted to enrich functions and molecular pathways of common targets and the STRING database was used to establish a protein-protein interaction network (PPI). The effect of crocetin (CCT) on NAFLD was evaluated in a mouse model of NAFLD by measuring the biomarkers of lipid, liver and renal function, oxidative stress, and inflammation. Liver histopathology was performed to evaluate liver injury. Nuclear factor erythroid-related factor (Nrf2) and hemeoxygenase-1 (HO-1) were examined to elucidate underlying mechanism for the protective effect of saffron against NAFLD.Results: A total of nine bioactive ingredients of saffron, including CCT, with 206 common targets showed therapeutic effects on NAFLD. Oxidative stress and diabetes related signaling pathways were identified as the critical signaling pathways mediating the therapeutic effects of the active bioactive ingredients on NAFLD. Treatment with CCT significantly reduced the activities of aspartate aminotransferase (AST), alanine transaminase (ALT), and the levels of total cholesterol (TC), triglyceride (TG), malondialdehyde (MDA), blood urea nitrogen (BUN), creatinine (CR), and uric acid (UA). CCT significantly increased the activities of superoxide dismutase (SOD), and catalase (CAT). Histological analysis showed that CCT suppressed high-fat diet (HFD) induced fat accumulation, steatohepatitis, and renal dysfunctions. Results of ELISA assay showed that CCT decreased the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and increased the expression of HO-1 and Nrf2.Conclusion: This study shows that CCT is a potential bioactive ingredient of saffron that treats NAFLD. Its mechanism of action involves suppressing of oxidative stress, mitigating inflammation, and upregulating Nrf2 and HO-1 expression.