Black chokeberry (Aronia melanocarpa) fruits are rich in anthocyanins, which are vital secondary metabolites that possess antioxidative properties. The aim of this study was to isolate and purify the anthocyanins from black chokeberry by simulated moving bed (SMB) chromatography, and to investigate the neuroprotective effect of SMB purified anthocyanin against Aβ-induced memory damage in rats. The parameters of the SMB process were studied and optimized. Anthocyanin extracts were identified by HPLC and UPLC-QTOF-MS, and antioxidant abilities were evaluated. The Aβ-induced animal model was established by intracerebral ventricle injection in rat brain. Through the SMB purification, anthocyanins were purified to 85%; cyanidin 3-O-galactoside and cyanidin 3-O-arabinoside were identified as the main anthocyanins by UPLC-QTOF-MS. The SMB purified anthocyanins exhibited higher DPPH and ABTS free radical scavenging abilities than the crude anthocyanins extract. Furthermore, rats receiving SMB purified anthocyanins treatment (50 mg/kg) showed improved spatial memory in a Morris water maze test, as well as protection of the cells in the hippocampus against Aβ toxicity. These results demonstrate that anthocyanins could serve as antioxidant and neuroprotective agents, with potential in the treatment of Alzheimer’s disease.

Antioxidant activity and neuroprotective activity of three stilbenoids, namely, trans-4-hydroxystilbene (THS), trans-3,5,4′-trihydroxy-stilbene (resveratrol, RES), and trans-3′,4′,3,5-tetrahydroxy-stilbene (piceatannol, PIC), against β-amyloid (Aβ)-induced neurotoxicity in rat primary cortex neurons were evaluated. THS, RES, and PIC significantly scavenged DPPH• and •OH radicals. All three stilbenoids were able to inhibit Aβ neurotoxicity by decreasing intracellular reactive oxygen species (ROS) via the PI3K/Akt signalling pathway. Specifically, stilbenoids significantly promoted Akt phosphorylation; suppressed Bcl-2/Bax expression; and inhibited caspase-9, caspase-3, and PARP cleavage. Molecular docking between stilbenoids with Akt indicated that stilbenoids could form hydrogen bond interactions with the COOH-terminal region of Akt. Additionally, the neuroprotective activity of stilbenoids correlated with the number and position of hydroxyl groups. The lack of meta-dihydroxyl groups on THS did not affect its neuroprotective activity in comparison with RES, whereas the ortho-dihydroxyl moiety on PIC significantly enhanced neuroprotective activity. These results provide new insights into the correlation between the biological activity and chemical structure of stilbenoids.

Cyanidin 3-O-galactoside (Cy3Gal) fromAronia melanocarpaand coadministration of metformin had a neuroprotective effect and alleviated cognitive impairment in the SAMP8 mice, and regulated the metabolites in feces and urine.

Enteromorpha prolifera (EP) is a green alga that causes green bloom worldwide. This study aimed to isolate and identify n-3 polyunsaturated fatty acids (PUFAs) from EP oil obtained via supercritical fluid extraction (SFE) and to explore its preventive effects against dextran sodium sulfate (DSS)-induced ulcerative colitis in C57BL/6J mice. In EP oil, we found the novel n-3 polyunsaturated fatty acid C16:4n-3 and two unusual fatty acids C18:4n-3 and C16:3n-3, using GC-MS. The administration of EP oil reduced histopathological of symptoms colitis and the shortening of the colon length. Pro-inflammatory cytokines of IL-6 and TNF-α in serum of EP oil treatment were lower than DSS treatment (by 37.63% and 83.52%), and IL-6 gene expression in the colon was lower in than DSS group by 48.28%, and IL-10 in serum was higher than DSS group by 2.88-fold. Furthermore, the protein expression of p-STAT3 by the EP oil treatment was significantly reduced compared with DSS treatment group by 73.61%. Lipidomics study suggested that phosphatidylcholine and phosphatidylethanolamine were positively associated with the anti-inflammatory cytokine IL-10, while cholesteryl ester and sphingomyelin were negatively related to inflammation cytokines in the EP oil group. The present results indicated that EP oil rich in n-3 PUFA contains a novel fatty acid C16:4n-3, as well as two uncommon fatty acids C18:4n-3 and C16:3n-3. EP oil could prevent DSS-induced ulcerative colitis by regulating the JAK/STAT pathway and lipid metabolism.

Objectives: This study explored whether the combined administration of niacin and B. animalis subsp. lactis F1-7 exerts a protective effect against alcohol-induced liver injury via the gut-liver axis, with a specific focus on the HCAR2-NLRP3 signaling pathway, and further investigated the functional roles of gut microbiota and metabolites. Methods: A mouse model of alcoholic fatty liver disease was established via chronic ethanol feeding with the Lieber–DeCarli liquid diet. Experimental animals were divided into six intervention groups: control group, model group, niacin alone, F1-7 alone, combined niacin and F1-7 (NF), and antibiotic pretreatment followed by NF intervention. Results: The NF intervention significantly improved serum lipids, reduced ALT/AST, alleviated hepatic steatosis and inflammation, and restored intestinal barrier integrity, while upregulating HCAR2 and suppressing NLRP3 activation; these effects were largely abolished by antibiotics. The 16S rRNA sequencing revealed that NF intervention reshaped the gut microbiota, enriching beneficial genera such as Lactobacillus, Bifidobacterium, and Faecalibaculum. Untargeted metabolomics showed that NF intervention enriched the ketone body β-hydroxybutyrate, which was positively correlated with the abundance of beneficial bacteria; this metabolite was identified as a key node in the ketone-body synthesis/degradation pathway and ranked among the top differential metabolites by VIP score. Conclusions: The combination additively alleviates alcohol-induced hepatic and intestinal injury in a gut microbiota-dependent manner. Intestinal β-hydroxybutyrate was enriched following the combined intervention in a microbiota-dependent fashion, and this enrichment was associated with HCAR2 activation and NLRP3 inhibition. These findings demonstrate that the protective action is largely dependent on an intact gut microbiota and support the combined intervention as a promising strategy against alcoholic liver disease.