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1.
Ecotoxicol Environ Saf ; 204: 111034, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32758695

RESUMO

Trehalose is the major blood sugar in insects; it not only serves as an energy source but also plays important roles in physiological responses to adverse conditions. However, only a few studies have explored the effects of heavy metal exposure stress on trehalose metabolism in insects. Therefore, in this study, we examined the effects of cadmium stress on changes in trehalose metabolism in Aedes albopictus. Three concentrations of cadmium (0.005, 0.01, and 0.1 mg/L) were selected for evaluation of long-term stress in Ae. albopictus (from eggs to adults); Ae. albopictus in double-distilled water was used as the control group. The trehalose and glucose contents, trehalase activity, and trehalose metabolism-related gene expression were determined. The effects of long-term cadmium exposure on growth, development, and reproduction were also assessed. Trehalose contents were increased, whereas glucose contents and trehalase activity were decreased in Ae. albopictus following long-term exposure to low concentrations of cadmium compared with those in untreated individuals. Moreover, the expression of trehalose-6-phosphate synthase was upregulated, and that of trehalase was downregulated, indicating that Ae. albopictus may enhance trehalose synthesis to resist cadmium stress. Cadmium exposure also caused Ae. albopictus individuals to become smaller with a longer developmental duration, whereas both reproduction and hatching rates of the offspring were decreased compared with those in the control group. Our findings demonstrated that cadmium exposure affected the morphology, physiology, and biochemistry of Ae. albopictus. These findings also confirmed the role of trehalose in the response of Ae. albopictus to cadmium stress, providing insights into the effects of heavy metal stress on trehalose metabolism in an insect model.


Assuntos
Aedes/efeitos dos fármacos , Cádmio/efeitos adversos , Trealose/metabolismo , Poluentes Químicos da Água/efeitos adversos , Aedes/crescimento & desenvolvimento , Aedes/metabolismo , Animais , Feminino , Larva/efeitos dos fármacos , Larva/crescimento & desenvolvimento , Larva/metabolismo , Óvulo/efeitos dos fármacos , Óvulo/crescimento & desenvolvimento , Óvulo/metabolismo , Pupa/efeitos dos fármacos , Pupa/crescimento & desenvolvimento , Pupa/metabolismo
2.
J Ethnopharmacol ; 248: 112361, 2020 Feb 10.
Artigo em Inglês | MEDLINE | ID: mdl-31683033

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: The traditional Chinese medicine Forsythiae Fructus is the dried fruit of Forsythia suspensa (Thunb.) Vahl. It is commonly used to clear heat and detoxify, reduce swelling and disperse knot, and evacuate wind and heat. AIM OF THE STUDY: Inflammation is involved in liver fibrosis. Phillygenin (PHI) is a kind of lignans extracted and separated from Forsythiae Fructus, which has been reported to have a good anti-inflammatory effect. Therefore, we aimed to explore whether PHI has a therapeutic effect on liver fibrosis caused by inflammation. MATERIALS AND METHODS: Firstly, the induction of the LX2 cells inflammatory model and fibrosis model by LPS with different concentrations were studied. Then, high, medium and low doses PHI was given for intervention therapy. The secretion of IL-6, IL-1ß and TNF-α inflammatory factors were detected by ELISA kit, and the expression of collagen I and α-SMA was detected by Western blot and RT-qPCR. The possible mechanism of PHI on TLR4/MyD88/NF-κB signal pathway was studied by computer-aided drug design software and the results were further verified by Western blot and RT-qPCR experiments. RESULTS: The results showed that LPS could promote the expression of IL-6, IL-1ß and TNF-α and the expression of collagen I and α-SMA, indicating that LPS could induce inflammation and fibrosis in LX2 cells. PHI could inhibit LX2 cell activation and fibrotic cytokine expression by inhibiting LPS-induced pro-inflammatory reaction. Molecular docking results showed that PHI could successfully dock with TLR4, MyD88, IKKß, p65, IκBα, and TAK1 proteins. Subsequently, Western blot and qPCR results further proved that PHI could inhibit the proteins expression in TLR4/MyD88/NF-κB signal pathway which were consistent with the molecular docking results. CONCLUSION: PHI can inhibit LPS-induced pro-inflammatory reaction and LX2 cell activation through TLR4/MyD88/NF-κB signaling pathway, thereby inhibiting liver fibrosis.


Assuntos
Anti-Inflamatórios/farmacologia , Células Estreladas do Fígado/efeitos dos fármacos , Hepatite/prevenção & controle , Lignanas/farmacologia , Lipopolissacarídeos/toxicidade , Cirrose Hepática/prevenção & controle , Fator 88 de Diferenciação Mieloide/metabolismo , NF-kappa B/metabolismo , Receptor 4 Toll-Like/metabolismo , Actinas/metabolismo , Linhagem Celular , Colágeno Tipo I/metabolismo , Células Estreladas do Fígado/metabolismo , Células Estreladas do Fígado/patologia , Hepatite/metabolismo , Hepatite/patologia , Humanos , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Cirrose Hepática/metabolismo , Cirrose Hepática/patologia , Transdução de Sinais , Fator de Necrose Tumoral alfa/metabolismo
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