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.

Accumulating clinical and epidemiological evidence indicates a close relationship between diabetes mellitus and dementia. The ginsenoside compound K (CK) has been reported to ameliorate diabetes mellitus and confer protection to the central nervous system. In this study, we investigated whether CK could improve memory impairment and cognitive dysfunction in diabetic db/db mice. Firstly, we found that CK treatments significantly improved behavioral impairment and cognitive dysfunction based on Morris water maze, Y-maze, and fear conditioning tests. Besides, CK decreased the fasting glucose level, increased lipid metabolism, and ameliorated glucose tolerance, insulin sensitivity, and dyslipidemia in diabetic db/db mice. In addition, CK treatments alleviated oxidative stress and inhibited the inflammatory response in hippocampal tissue. Further investigations showed that CK treatments inhibited the NLRP3 inflammasome pathway, as evidenced by the declined expression of TXNIP, NLRP3 inflammasomes, ASC, cleaved caspase-1, and mature IL-1β in hippocampal tissues. Moreover, CK treatments alleviated ER stress via down-regulating the level of BiP, CHOP, p-PERK, p-IRE1α and ATF6 in the hippocampus of db/db mice. These results suggest that CK improves memory and cognitive dysfunction, possibly by ameliorating glucose tolerance, insulin sensitivity, and dyslipidemia, suppressing oxidative stress and inflammatory response and modulating the NLRP3 inflammasome pathway and ER stress.

The aim of this study was to investigate the anti‐inflammatory property of the ethanol extract of the root and rhizome of Pogostemon cablin (ERP). The anti‐inflammatory effect was evaluated using four animal models including xylene‐induced mouse ear edema, acetic acid‐induced mouse vascular permeability, carrageenan‐induced mouse pleurisy, and carrageenan‐induced mouse hind paw edema. Results indicated that oral administration of ERP (120, 240, and 480 mg/kg) significantly attenuated xylene‐induced ear edema, decreased acetic acid‐induced capillary permeability, inhibited carrageenan‐induced neutrophils recruitment, and reduced carrageenan‐induced paw edema, in a dose‐dependent manner. Histopathologically, ERP (480 mg/kg) abated inflammatory response of the edema paw. Preliminary mechanism studies demonstrated that ERP decreased the level of MPO and MDA, increased the activities of anti‐oxidant enzymes (SOD, GPx, and GRd), attenuated the productions of TNF‐α, IL‐1β, IL‐6, PGE₂ and NO, and suppressed the activities of COX‐2 and iNOS. This work demonstrates that ERP has considerable anti‐inflammatory potential, which provided experimental evidences for the traditional application of the root and rhizome of Pogostemon cablin in inflammatory diseases.

The aim of this study was to analyze the chemical composition and investigate the anti-inflammatory property of the supercritical-carbon dioxide extract from flowers and buds ofC. indicum(CI_SCFE). The anti-inflammatory effect was evaluated in four animal models including xylene-induced mouse ear edema, acetic acid-induced mouse vascular permeability, carrageenan-induced mouse hind paw edema, and cotton pellet-induced rat granuloma formation. The results indicated that CI_SCFEsignificantly attenuated xylene-induced ear edema, decreased acetic acid-induced capillary permeability, reduced carrageenan-induced paw, and inhibited the cotton pellet-induced granuloma formation in a dose-dependent manner. Histopathologically, CI_SCFEabated inflammatory response of the edema paw. Preliminary mechanistic studies demonstrated that CI_SCFEdecreased the MDA level via increasing the activities of anti-oxidant enzymes (SOD, GPx, and GRd), attenuated the productions of NF-κB, TNF-α, IL-1β, IL-6, PGE₂and NO, and suppressed the activities of iNOS and COX-2. In phytochemical study, 35 compounds were identified by GC-MS, and 5 compounds (chlorogenic acid, luteolin-7-glucoside, linarin, luteolin and acacetin) were reconfirmed and quantitatively determined by HPLC-PAD. This paper firstly analyzed the chemical composition by combining GC-MS with HPLC-PAD and explored possible mechanisms for the anti-inflammatory effect of CI_SCFE.

The aim of the present study was to explore whether the supercritical-carbon dioxide fluid extract from flowers and buds of Chrysanthemum indicum (SEC) exhibits antidepressant-like effects in a chronic unpredictable mild stress (CUMS)-induced mice model. Firstly, SEC was found to reverse a CUMS-induced decrease in the body weight gain in mice. Next, SEC was found to alleviate CUMS-induced depressive-like behavior, evidenced by the reversal of the decrease in the sucrose consumption in the sucrose preference test (SPT), the increase in the locomotor activity in the open field test (OPF), and the alleviation of immobility duration in both the forced swimming test (FST), and tail-suspension test (TST). SEC also attenuated CUMS-induced hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis by decreasing the levels of serum corticosterone and (CORT) and adrenocorticotropic hormone (ACTH), and hypothalamus corticotrophin-releasing hormone (CRH). In addition, SEC was found to suppress the expression of pro-inflammatory cytokines, including the tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the hippocampal of CUMS mice. Interestingly, further investigations demonstrated that SEC inhibited CUMS-induced activation of the nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasomes pathways but upregulated brain-derived neurotrophic factor (BDNF) expression and promoted phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP-response element-binding protein (CREB) in hippocampal. In summary, SEC was able to alleviate depressive-like behavior in a CUMS-induced mice model, accompanied by inhibitory roles in the hyperactivity of the HPA axis and pro-inflammatory cytokine expression. Modulating the NF-κB/NLRP3 and BDNF/CREB/ERK pathways contributed to SEC-mediated antidepressant-like effects.

The supercritical-carbon dioxide fluid extract ofChrysanthemum indicumLinné. (CFE) has been demonstrated to be effective in suppressing inflammation. The aim of this study is to investigate the preventive action and underlying mechanisms of CFE on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. ALI was induced by intratracheal instillation of LPS into lung, and dexamethasone was used as a positive control. Results revealed that pretreatment with CFE abated LPS-induced lung histopathologic changes, reduced the wet/dry ratio and proinflammatory cytokines productions (TNF-α, IL-1β, and IL-6), inhibited inflammatory cells migrations and protein leakages, suppressed the levels of MPO and MDA, and upregulated the abilities of antioxidative enzymes (SOD, CAT, and GPx). Furthermore, the pretreatment with CFE downregulated the activations of NF-κB and the expressions of TLR4/MyD88. These results suggested that CFE exerted potential protective effects against LPS-induced ALI in mice and was a potential therapeutic drug for ALI. Its mechanisms were at least partially associated with the modulations of TLR4 signaling pathways.