The effect of polysaccharides isolated from Dendrobium officinale (DOP) on acetaminophen‐ (APAP‐) induced hepatotoxicity and the underlying mechanisms involved are investigated. Male Institute of Cancer Research (ICR) mice were randomly assigned to six groups: (1) control, (2) vehicle (APAP, 230 mg/kg), (3) N‐acetylcysteine (100 mg/kg), (4) 50 mg/kg DOP, (5) 100 mg/kg DOP, and (6) 200 mg/kg DOP. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the serum and glutathione (GSH), malondialdehyde (MDA), catalase (CAT), total antioxidant capacity (T‐AOC), myeloperoxidase (MPO), and reactive oxygen species (ROS) levels in the liver were determined after the death of the mice. The histological examination of the liver was also performed. The effect of DOP on the Kelch‐like ECH‐associated protein 1‐ (Keap1‐) nuclear factor erythroid 2‐related factor 2 (Nrf2) signaling pathway was evaluated using Western blot analysis and real‐time polymerase chain reaction (PCR). The results showed that DOP treatment significantly alleviated the hepatic injury. The decrease in ALT and AST levels in the serum and ROS, MDA, and MPO contents in the liver, as well as the increases in GSH, CAT, and T‐AOC in the liver, were observed after DOP treatment. DOP treatment significantly induced the dissociation of Nrf2 from the Nrf2−Keap1 complex and promoted the Nrf2 nuclear translocation. Subsequently, DOP‐mediated Nrf2 activation triggered the transcription and expressions of the glutamate–cysteine ligase catalytic (GCLC) subunit, glutamate–cysteine ligase regulatory subunit (GCLM), heme oxygenase‐1 (HO‐1), and NAD(P)H dehydrogenase quinone 1 (NQO1) in APAP‐treated mice. The present study revealed that DOP treatment exerted potentially hepatoprotective effects against APAP‐induced liver injury. Further investigation about mechanisms indicated that DOP exerted the hepatoprotective effect by suppressing the oxidative stress and activating the Nrf2−Keap1 signaling pathway.

The study aimed to evaluate the protective effect of Dendrobium officinale flower extraction (DOFE) on alcohol‐induced liver injury and its probable mechanisms in mice. The chemical composition of DOFE was performed via UPLC/MS. Male Kunming mice were used to establish alcohol‐induced liver injury models by oral gavage of 56% alcohol. Results showed that DOFE dramatically attenuated the increased serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), and triacylglycerol (TG). Meanwhile, hematoxylin and eosin and Oil Red O staining showed that DOFE attenuated degeneration, inflammatory infiltration, and lipid droplet accumulation. DOFE was also found to suppress the activity of malonaldehyde (MDA) and enhanced the level of glutathione (GSH) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and catalase (CAT) in the liver. The protection of DOFE against oxidative stress was associated with the downregulation of hepatic cytochrome P450 2E1 (CYP2E1) and upregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1), and NAD(P)H quinone oxidoreductase l (NQO1). Additionally, DOFE suppressed inflammation via downregulating Toll‐like receptor‐4 (TLR‐4) and nuclear factor kappa‐B P65 (NF‐κB P65). Thus, DOFE exhibited a significant protective effect against alcohol‐induced liver injury through its antisteatosis, antioxidative, and anti‐inflammatory effect.

Two new pentacyclic triterpene saponins, named akebiaoside K (1) and akebiaoside N (2), were isolated from the leaves of Akebia trifoliata, together with five known triterpenoids 3–7. They were all isolated from the leaves of A. trifoliata for the first time. Their structures were established by spectral and chemical means. Triterpenes 5 and 7 were found to show moderate in vitro cytotoxicity against human tumor A549, HeLa and HepG2 cell lines, with IC₅₀ values ranging from 0.023 to 0.038 mM. Triterpenes 5–7 were further revealed to show significant in vitro α-glucosidase inhibitory activity with IC₅₀ values from 0.040 to 0.220 mM, making them more potent than the reference compound acarbose (IC₅₀ 0.409 mM). Meanwhile, no obvious inhibitory effects were observed for the isolated triterpene saponins 1–4 in both bioactivity assays.

Dihydrochalcones (DHCs) constitute a specific class of flavonoids widely known for their various health-related advantages. Melatonin (MLT) has received attention worldwide as a master regulator in plants, but its roles in DHC accumulation remain unclear. Herein, the elicitation impacts of MLT on DHC biosynthesis were examined in Lithocarpus litseifolius, a valuable medicinal plant famous for its sweet flavor and anti-diabetes effect. Compared to the control, the foliar application of MLT significantly increased total flavonoid and DHC (phlorizin, trilobatin, and phloretin) levels in L. litseifolius leaves, especially when 100 μM MLT was utilized for 14 days. Moreover, antioxidant enzyme activities were boosted after MLT treatments, resulting in a decrease in the levels of intracellular reactive oxygen species. Remarkably, MLT triggered the biosynthesis of numerous phytohormones linked to secondary metabolism (salicylic acid, methyl jasmonic acid (MeJA), and ethylene), while reducing free JA contents in L. litseifolius. Additionally, the flavonoid biosynthetic enzyme activities were enhanced by the MLT in leaves. Multiple differentially expressed genes (DEGs) in RNA-seq might play a crucial role in MLT-elicited pathways, particularly those associated with the antioxidant system (SOD, CAT, and POD), transcription factor regulation (MYBs and bHLHs), and DHC metabolism (4CL, C4H, UGT71K1, and UGT88A1). As a result, MLT enhanced DHC accumulation in L. litseifolius leaves, primarily by modulating the antioxidant activity and co-regulating the physiological, hormonal, and transcriptional pathways of DHC metabolism.

The aim of this study was to investigate the hepatoprotective effect of ultrafine powder of Dendrobium officinale (UDO) against acetaminophen (APAP)-induced liver injury in mice. ICR mice were orally administered with UDO (100, 200, 400 mg/kg/day) for 14 days before intraperitoneal injection of APAP. The results showed that UDO exhibited a significant dose-dependently preventive effect on APAP-induced hepatotoxicity. Pretreatment with UDO significantly reduced the serum levels of alanine transaminase and aspartate aminotransferase. Histological examination indicated that administration with UDO alleviated inflammation and necrosis as well as ameliorated hepatocyte steatosis, especially at 200 and 400 mg/kg doses. Additionally, UDO markedly recovered the activities of glutathione, catalase and total antioxidant capacity, and decreased the content of malonaldehyde and reactive oxygen species. In summary, the results suggested that pretreatment with UDO exists potently hepatoprotective effects against APAP-induced liver damage, which may be related to the enhanced antioxidant capacity and inhibited lipid peroxidation.