atractylon and Disease-Models--Animal

Motor symptoms of Parkinson's disease (PD) are characterized by bradykinesia, resting tremor, rigidity, slow movement, impaired gait and postural instability, resulting from progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Atractylon is a natural furan compound in Atractylodes rhizomes, exhibiting anticancer, anti-inflammation, antiviral and gastroprotective activities, and so on. However, it is still unknown whether atractylon is beneficial to motor dysfunctions of PD.. GPCR-targeted piggyBac-TANGO compound screening system, cAMP assay, and immunostaining of p-CREB and BDNF were used to identify dopamine 2 receptor (DRD2) activation. The effects of atractylon on motor deficits and gait disturbances, as well as tyrosine hydroxylase (TH) in the SNpc were investigated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice.. Atractylon treatment increased the eGFP expression in dose-dependent manner in piggyBac-TANGO assay, decreased cAMP production, and enhanced the levels of p-CREB and BDNF in DRD2 highly expresseding SY-SY5Y cells. In MPTP-induced mice, atractylon improved the slow movement, diminished voluntary locomotion, and abnormal gait parameters, such as duration, cadence, average speed, step cycle, stride length, and so on. Moreover, atractylon rescued the TH positive cells in SNpc and TH positive nerve fibers in striatum.. Atractylon could effectively activate DRD2, attenuate motor deficits and gait disorders, and protect dopaminergic neurons in MPTP-induced PD mice. Our findings stretch out the therapeutic potential of atractylon for motor symptoms of PD.

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Corpus Striatum; Disease Models, Animal; Dopamine Agonists; Dopaminergic Neurons; Mice; Mice, Inbred C57BL; Parkinsonian Disorders; Sesquiterpenes; Substantia Nigra; Tyrosine 3-Monooxygenase

The aim of the present study was to investigate the molecular mechanisms of atractylon in the inhibition of invasion and migration of hepatic cancer cells. High‑throughput sequencing was used to compare the expression of long non‑coding (lnc)RNAs between hepatic carcinoma and healthy controls. A competing endogenous RNA network was constructed. The top significantly differentially expressed lncRNAs were screened and verified by reverse transcription‑quantitative PCR

Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Movement; Cell Proliferation; Disease Models, Animal; Female; Gene Expression Regulation, Neoplastic; Hep G2 Cells; High-Throughput Nucleotide Sequencing; Humans; Liver Neoplasms; Male; Mice, Inbred BALB C; Mice, Nude; RNA, Long Noncoding; RNA, Small Interfering; Sequence Analysis, RNA; Sesquiterpenes

Chronic intermittent hypoxia (CIH) induced by sleep-disordered breathing (SDB) is a key factor involved in cognitive dysfunction (CD). Increasing evidence has shown that atractylon (ATR) has anti-inflammatory effects. However, it remains unclear if ATR has a protective effect against SDB-induced nerve cell injury and CD. So, in the present study, CIH-exposed mice and CIH-induced BV2 cells were used to mimic SDB. The results showed that ATR treatment decreased CIH-induced CD and the expression of inflammatory factors in the hippocampal region by suppression of M1 microglial activation and promotion of M2 microglial activation. Also, ATR treatment promoted sirtuin 3 (SIRT3) expression. Down-regulation of SIRT3 decreased the protective effect of ATR against CIH-induced microglial cell injury. Furthermore, in vitro detection found that SIRT3 silencing suppressed ATR-induced M2 microglial activation after exposure to CIH conditions. Taken together, these results indicate that ATR treatment prevents SDB-induced CD by inhibiting CIH-induced M1 microglial activation, which is mediated by SIRT3 activation.

Topics: Animals; Anti-Inflammatory Agents; Behavior, Animal; Cell Line; Chronic Disease; Cognition; Cognitive Dysfunction; Cytokines; Disease Models, Animal; Enzyme Activation; Hippocampus; Hypoxia; Inflammation Mediators; Mice, Inbred BALB C; Microglia; Morris Water Maze Test; Phenotype; Sesquiterpenes; Sirtuin 3; Sleep Apnea Syndromes

KMP6 (Pyeongwee-San) is a Korean Medicine used to treat gastrointestinal disorders. Recently, we reported KMP6 had beneficial effects on allergic inflammatory diseases. The aim of this study was to evaluate the effects of atractylone (Atr), a constituent of KMP6, on allergic rhinitis (AR) and to identify the mechanism responsible for these effects. The anti-allergic inflammatory effects of Atr were evaluated on phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-stimulated human mast cell line, HMC-1 cells and in an ovalbumin (OVA)-induced AR animal model using Western blotting, quantitative real-time PCR, ELISA, and immunohistochemistry methods. In HMC-1 cells, Atr and KMP6 attenuated PMACI-caused proinflammatory cytokine production and mRNA expression. We found that PMACI induced caspase-1/nuclear factor (NF)-κB/mitogen activated protein kinases (MAPKs) activation. PMACI-caused caspase-1/NF-κB/MAPKs activations were attenuated by Atr and KMP6. In AR animal model, Atr and KMP6 reduced AR clinical symptoms and biomarkers including rub scores, total IgE, histamine, prostaglandin D

Topics: Animals; Blotting, Western; Cells, Cultured; Chromatography, Liquid; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immunohistochemistry; Inflammation; Mast Cells; Mice; Mice, Inbred BALB C; Nasal Mucosa; Plant Extracts; Real-Time Polymerase Chain Reaction; Rhinitis, Allergic; Sesquiterpenes; Tandem Mass Spectrometry