Reactive oxygen species (ROS) modulate nitrogen signaling using temporal transcriptome analysis in foxtail millet.

Reactive oxygen species (ROS) is a chemically reactive chemical substance containing oxygen and a natural by-product of normal oxygen metabolism. Excessive ROS affect the growth process of crops, which will lead to the decrease of yield. Nitrogen, as a critical nutrient element in plants and plays a vital role in plant growth and crop production. Nitrate is the primary nitrogen source available to plants in agricultural soil and various natural environments. However, the molecular mechanism of ROS-nitrate crosstalk is still unclear. In this study, we used the foxtail millet (Setaria italica L.) as the material to figure it out. Here, we show that excessive NaCl inhibits nitrate-promoted plant growth and nitrogen use efficiency (NUE). NaCl induces ROS accumulation in roots, and ROS inhibits nitrate-induced gene expression in a short time. Surprisingly, low concentration ROS slight promotes and high concentration of ROS inhibits foxtail millet growth under long-term H2O2 treatment. These results may open a new perspective for further exploration of ROS-nitrate signaling pathway in plants.

[Effect of shikonin on proliferation of keratinocytes induced by interleukin-17 and expression of chemokines].

OBJECTIVE: To observe the effect of shikonin on the proliferation of human keratinocytes induced by IL-17 and secretion of chemokines, in order to discuss the mechanism of Shikonin in the treatment of psoriasis. METHOD: In vitro cultured HaCaT cells were stimulated by IL-17A (200 µg x L(-1)) and mixed with different concentrations (2, 1 mg x L(-1)) of shikonin for 24 hours. The cell proliferation was detected by CCK-8 assay. Cell secretion inflammatory factor interleukin-23 (IL-23) was detected by ELISA. The expressions of intracellular chemokines CXCL1, CXCL2, CCL20 and 6-defensin 4 (DEFB4) were detected by Real-time PCR. RESULT: Shikonin (2,1 mg x L(-1)) could distinctly inhibit HaCaT cell proliferation induced by IL-17A, with statistical difference (P < 0.01). Each shikonin group showed decreases in the secretion of IL-23 and inhibition in expressions of intracellular CXCL1, CXCL2, CCL20 and DEFB4. CONCLUSION: Shikonin could inhibit HaCaT cells proliferation induced by IL-17 and secretion of relevant cytokines and recruit leukocytes by inhibiting chemokines, so as to show the effect in treating psoriasis.

[Effect of blood cooling and detoxification formula and its dismantled formulae on keratinocyte proliferation induced by activated T lymphocytes].

OBJECTIVE: To observe the effect of the blood cooling and detoxification formula and its dismantled formulae on activated T lymphocytes-induced keratinocyte proliferation and cytokine secretion. METHOD: Rat drug-containing serum was prepared. PDB-stimulated T lymphocytes and Colo-16 cells were co-cultured, then added with the drug-containing serum, and laid aside for 24 h. The cell proliferation was detected by MTT assay. Cytokines TNF-alpha, sICAM-1 and IFN-gamma were detected by ELISA. RESULT: The blood cooling and detoxification formula has a notable inhibitory effect on activated T lymphocyte-induced Colo-16 keratinocyte proliferation, with a significant difference between the whole formula group and the blood cooling group (P < 0.01). After activated T lymphocytes had added into Colo-16 cells for 24 hour, sICAM-1, TNF-alpha and IFN-gamma significantly increased. Though the whole blood cooling and detoxification formula, the blood cooling formula and the detoxification formula could notably reduce sICAM-1, TNF-alpha, IFN-gamma, the whole formula group showed the most significant effect. CONCLUSION: The blood cooling and detoxification formula, as an effective traditional Chinese medicine compound for clinical treatment of psoriasis, can significantly inhibit activated T lymphocyte-induced keratinocyte proliferation and cytokine secretion.

[Effect of berberine on left ventricular remodeling in renovascular hypertensive rats].

The purpose of this study is to evaluate the effects and the underline mechanisms of berberine on the cardiac function and left ventricular remodeling in rats with renovascular hypertension. The renovascular hypertensive model was established by the two-kidney, two-clip (2K2C) method in Sprague-Dawley (SD) rats. Two weeks after surgery, all the operated SD rats were randomly assigned into four groups: (1) renovascular hypertensive model group; (2) berberine 5 mg x kg(-1) group; (3) berberine 10 mg x kg(-1) group; (4) captopril 45 mg x kg(-1) group; and the sham operated rats were used as control. Four weeks after the drugs were administered, the cardiac function was assessed. The ratios of heart weight to body weight (HW/BW), left ventricular weight to body weight (LVW/BW) and right ventricular weight to body weight (RVW/BW) were compared between groups. Coronal sections of the left ventricular tissue (LV) were prepared for paraffin sections, picrosirius red and HE staining was performed. The left ventricular wall thickness (LVWT), interventricular septal thickness (IVST), the parameters of myocardial fibrosis indicated by interstitial collagen volume fraction (ICVF) and perivascular collagen area (PVCA) were assessed. Nitric oxide (NO), adenosine cyclophosphate (cAMP) and guanosine cyclophosphate (cGMP) concentrations of left ventricular tissue were measured. Berberine 5 mg x kg(-1) and 10 mg x kg(-1) increased the left ventricular +/- dp/dt(max) and HR. Berberine 10 mg x kg(-1) decreased HW/BW and LVW/BW. The image analysis showed that both 5 and 10 mg x kg(-1) of berberine decreased LVWT, ICVF and PVCA, while increased the NO and cAMP contents in left ventricular tissue. Berberine could improve cardiac contractility of 2K2C model rats, and inhibit left ventricular remodeling especially myocardial fibrosis in renovascular hypertension rats. And such effects may partially associate with the increased NO and cAMP content in left ventricular tissue.