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2.
Ying Yong Sheng Tai Xue Bao ; 32(7): 2496-2504, 2021 Jul.
Article in English | MEDLINE | ID: mdl-34313068

ABSTRACT

We examined the effects of exogenous melatonin (MT) on the resistance of Chrysanthemum morifolium 'Jinba' to high temperature stress. Chrysanthemum leaves were sprayed with 200 µmol·L-1MT, and then subjected to high temperature stress at 40 ℃ (day)/ 35 ℃ (night). The ultrastructure of chloroplast and thylakoid of chrysanthemum leaves were observed, and the photosynthetic and physiological indices were measured. The results showed that the chloroplast and thyla-koid structures of chrysanthemum were damaged under high temperature stress. The chlorophyll contents and maximum fluorescence (Fm) were significantly reduced, while the OJIP curve changed with the fluorescence of K and J points increased. The net photosynthetic rate (Pn), transpiration rate (Tr) and stomatal conductance (gs) were significantly decreased, while the internal CO2 concentration (Ci) was significantly increased. The relative conductivity (REC), malondialdehyde (MDA), reactive oxygen species (ROS), osmotic adjustment substances content and antioxidant enzyme activity all increased significantly. Spraying exogenous MT onto leaves could maintain the integrity of chloroplast and thylakoid structure under high temperature in chrysanthemum and significantly decrease the increment in the K and J points of OJIP curve. Exogenous application of MT alleviated the inhibition of high temperature stress on photosynthesis and fluorescence of chrysanthemum, as indicated by significantly higher Fm, Pn, gs, Tr and photosynthetic pigment contents and lower Ci. Exogenous MT also significantly reduced the REC, MDA and ROS contents of chrysanthemum under high temperature stress, and enhanced the osmotic adjustment substances content and antioxidant enzyme activity in chrysanthemum leaves. It suggested that exogenous MT could protect the integrity of chloroplast structure of chrysanthemum leaves, enhance photosynthesis, inhibit the excessive production of ROS in the plants under high temperature stress, improve the activity of antioxidant enzyme system, reduce the level of membrane peroxidation and keep the integrity of lipid membrane, and thus improve the ability of chrysanthemum plants to resist high temperature stress.


Subject(s)
Melatonin , Seedlings , Chlorophyll , Melatonin/pharmacology , Photosynthesis , Plant Leaves , Stress, Physiological , Temperature
3.
Int J Mol Med ; 33(6): 1498-506, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24714963

ABSTRACT

Apoptosis plays a role in the normal development of liver. However, overactivation thereof may lead to hepatocellular damage. The aim of this study was to assess D-galactosamine (D-GalN)/lipopolysaccharide (LPS)-induced hepatocyte apoptotic changes in mice and clarify the mechanisms involved in this process. DNA ladder detection was employed to determine the induction condition of hepatic apoptosis. An initial test indicated that typical hepatocyte apoptosis was observed at 6-10 h after the intraperitoneal injection of D-GalN (700 mg/kg) and LPS (10 µg/kg). Subsequently, we evaluated hepatocyte apoptosis at 8 h after administering D-GalN/LPS by histopathological analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end­labeling (TUNEL) detection, flow cytometry and electron microscopy analysis. To clarify the apoptosis-related gene expression, the expression levels of tumor necrosis factor-α (TNF-α), transforming growth factor-ß1 (TGF-ß1), caspase-3, and Fas/Fas ligand (FasL) were determined by serum enzyme immunoassay, immunohistochemistry and western blot analysis. Strong apoptotic positive signals following D-GalN/LPS injection were observed from the results of the serum analysis, histopathological and immunohistochemical analyses, DNA ladder detection, TUNEL detection, flow cytometry and electron microscopy analysis. Additionally, apoptotic hepatocytes were mainly at the late stage of cell apoptosis. The expression of TNF-α, TGF-ß1, caspase-3 and Fas/FasL was significantly increased. In conclusion, this study evaluated the D-GalN/LPS-induced hepatocyte apoptotic changes and clarified the apoptosis-related gene expression in mice. The hepatocyte apoptosis induced by D-GalN/LPS may be mainly regulated by the death receptor pathway. TGF-ß signaling pathway may also play a vital role in this process of hepatocyte apoptosis.


Subject(s)
Apoptosis/drug effects , Galactosamine/pharmacology , Hepatocytes/cytology , Hepatocytes/drug effects , Lipopolysaccharides/pharmacology , Animals , Caspase 3/metabolism , Fas Ligand Protein/metabolism , Immunohistochemistry , In Situ Nick-End Labeling , Male , Mice , Mice, Inbred ICR , Transforming Growth Factor beta1/blood , Transforming Growth Factor beta1/metabolism , Tumor Necrosis Factor-alpha/blood , Tumor Necrosis Factor-alpha/metabolism
4.
J Ethnopharmacol ; 144(1): 190-4, 2012 Oct 31.
Article in English | MEDLINE | ID: mdl-22982394

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: The aim of this study was to determine the anti-hepatitis B effect of isochlorogenic acid A isolated from Laggera alata (Asteraceae), a traditional Chinese herbal medicine. MATERIALS AND METHODS: The anti-hepatitis B activity of isochlorogenic acid A was evaluated by the D-galactosamine (D-GalN)-induced HL-7702 hepatocyte damage model and the HBV-transfected HepG2.2.15 cells. RESULTS: Isochlorogenic acid A significantly improved HL-7702 hepatocyte viability and markedly inhibited the productions of HBsAg and HBeAg. The inhibitory rates of isochlorogenic acid A on the HBsAg and HBeAg expressions were 86.9% and 72.9%, respectively. In addition, isochlorogenic acid A declined markedly the content of hepatitis B virus covalently closed circular DNA (HBV cccDNA) and induced significantly the heme oxygenase-1 (HO-1) expression in HepG2.2.15 cells. CONCLUSIONS: Isochlorogenic acid A was verified to possess the potent anti-hepatitis B activity. The anti-HBV target of isochlorogenic acid A is probably associated with blocking the translation step of the HBV replication. Overexpression of HO-1 may contribute to the anti-HBV activity of isochlorogenic acid A by reducing the stability of the HBV core protein and thus blocking the refill of nuclear HBV cccDNA. Additionally, the hepatoprotective effect of isochlorogenic acid A could be achieved by its antioxidative property and induction of HO-1.


Subject(s)
Antiviral Agents/pharmacology , Asteraceae , Chlorogenic Acid/analogs & derivatives , Hepatitis B virus/drug effects , Protective Agents/pharmacology , Antigens, Viral/analysis , Cell Survival/drug effects , Chlorogenic Acid/pharmacology , DNA, Viral/analysis , Heme Oxygenase-1/metabolism , Hep G2 Cells , Hepatitis B/prevention & control , Hepatitis B virus/genetics , Humans
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