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To understand the mechanisms of agricultural ecosystem structure and function in response to soil water deficit under future elevated atmospheric CO2 concentration, we examined the effects of soil water deficit and elevated CO2 concentration ([CO2]) on the stomatal traits, leaf photosynthesis, water use efficiency as well as Rubisco activity and gene expression of winter wheat with environmental growth chambers, whereby the [CO2] was controlled accurately with CO2 sensors. Our results showed that water deficit significantly decreased the plant biomass and net photosynthesis rates (Pn) of winter wheat by 33% and 29%, whereas elevated [CO2] partially mitigated the negative effects of water deficit on plant growth and physiological processes of winter wheat. Meanwhile, water deficit also reduced the stomatal width and regularity of stomatal distribution pattern on winter wheat leaves, but higher [CO2] could optimize the leaf gas exchange efficiency with more regular distribution pattern of stomata. Moreover, elevated [CO2] not only enhanced the Pn of winter wheat plants under water deficit, but also substantially reduced the transpiration rates (Tr) by 25%, and thus elevated [CO2] increased the water use efficiency by 61% when winter wheat plants subjected to water deficit. In addition, elevated [CO2] boosted the initial activity and activation state of Rubisco as well as soluble protein content by 66%, 38%, and 15%, and meanwhile significantly enhanced the gene expression levels of RbcL3 and RbcS2 by 453% and 417%, respectively. These results suggested that elevated [CO2] may optimize leaf gas exchange through modifying stomatal traits as well as the activity and gene express of Rubisco, and thus increased plant biomass, Pn, and water use efficiency to efficiently alleviate the physiological stress of water deficit on growth and development processes of winter wheat. Our findings may not only provide data for further understanding the impacts of water deficit on grain yield and water use efficiency of winter wheat under elevated [CO2], but also have important significance for adaptation management of agricultural ecosystems under global change. [ABSTRACT FROM AUTHOR]

To the Editor, Group 2 innate lymphoid cells (ILC2s) produce the canonical type 2 cytokines interleukin (IL)-5 and IL-13 in response to epithelial cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP).[1] ILC2s have been to be involved in the pathogenesis of asthma, allergic rhinitis (AR) and atopic dermatitis (AD).[2] We have reported the higher ILC2 levels in patients with asthma and patients with AR.[[3]] Recently, the cysteinyl leukotriene (CysLT) D4 (LTD4) and LTE4 were reported to induce Th2 cytokine production from ILC2s.[[5]] LTE4 is the stable and dominant CysLT in the pathogenesis of allergic conditions. We found higher prevalence of ILC2s (Lin SP - sp CRTH2 SP + sp CD127 SP + sp cells, Figure A) and the higher expression of CysLT1R in ILC2s (Figure B-C B ) b from patients with AR compared to healthy controls. It suggests that the activation of ILC2s to LTC4, LTD4 but not LTE4 in AR is related to the increased expression of CysLT1R in AR, at least in our study. [Extracted from the article]

Puerarin has the anti-Alzheimer's disease (AD) activity,which can reverse nerve injury induced by Aβand inhibit neuronal apoptosis.However,its potential pharmacodynamic mechanism still needs to be further researched.The occurrence and development of AD is due to the change of multiple metabolic links in the body,which leads to the destruction of balance.Puerarin may act on multiple targets and multiple metabolic processes to achieve therapeutic purposes.Quantitative proteomic analysis provides a new choice to understand the mechanism as completely as possible.This research adopted SH-SY5Y cells induced by Aβ_(1-42)to establish AD cell model,and Aβimmunofluorescence detection showed that Aβdecreased significantly after puerarin intervention.The mechanism of puerarin reversing SH-SY5Y cell injured by Aβ_(1-42)was further explored by using label-free non-labeled quantitative technology and Western blot detection based on bioinformatics analysis result.The results showed that most of the differential proteins were related to biological processes such as cellular component organization or biogenesis,cellular component organization and cellular component biogenesis,and they mainly participated in the top ten pathways of P value such as pathogenic Escherichia coli infection,m TOR signaling pathway,regulation of autophagy,regulation of actin cytoskeleton,spliceosome,hepatocellular carcinoma,tight junction,non-small cell lung cancer,apoptosis and gap junction.Annexin V/PI flow cytometry and TUNEL were used to detect apoptosis,and the results showed that Aβdecreased significantly and the rate of apoptosis decreased significantly after puerarin intervention.Western blot analysis found that the protein expression level of autophagy related protein LC3Ⅱwas up-regulated after Aβinduction,and the degree of this up-regulation was further enhanced in puerarin intervention group.The trend of the ratio of LC3Ⅱ/LC3Ⅰamong groups was the same as the protein expression level of LC3Ⅱ，the protein expression level of p62 in the control group,AD model group and puerarin intervention group decreased successively.Protein interaction network analysis showed that CAP1 was correlated with TUBA1B,HSP90AB2P,DNM1L,TUBA1A and ERK1/2,and the correlation between CAP1 and ERK1/2 was the highest among them.Western blot showed that the expressions of p-ERK1/2,Bax and CAP1 were significantly down-regulated and the protein expression level of Bcl-2 was significantly up-regulated after puerarin intervention.Therefore,puerarin might improve the SH-SY5Y cells injured by Aβ_(1-42)through the interaction of multiple biological processes and pathways in cells multiple locations,and CAP1 might play an important role among them.

This study was designed to investigate the correlation between autophagy and polarization of macrophages in atherosclerosis (AS) plaque in arteriosclerosis obliterans amputees. Femoral artery specimens from arteriosclerosis obliterans amputees were performed hematoxylin and eosin (HE) staining, oil red O and immunofluorescence staining to observe the morphology of atherosclerotic plaque, phenotype of macrophages and autophagy in plaque; using real-time quantitative RT-PCR technology to detect the mRNA level of M1 and M2 type markers in arterial tissue; to analyze polarized signal pathway and autophagy protein levels in macrophages by Western blotting. Arterial specimens staining showed obvious lipid deposition and obvious infiltration of amount of foam cells and inflammatory cells. Macrophages were mainly expression M1 type in percentage in fibrous plaque. Although both M1 and M2 macrophages were upregulated in atheromatous plaque, the increase was dominant in M2 type in percentage. The level of autophagy was significantly higher in the atheromatous plaque than that of fibrous plaque. The expression of tumor necrosis factor- α (TNF-α), monocyte chemotactic protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and interleukin-12 (IL-12) mRNA was significantly higher in fibrous plaque than that of atheromatous plaque (P < 0.01 or 0.05), and arginase-1 (Arg-1), transforming growth factor-β (TGF-β), CD163 and interleukin-10 (IL-10) mRNA was significantly lower than that in atheromatous plaque (P < 0.01). The levels of p-STAT1 and NF-κB were significantly increased in fibrous plaque (P < 0.01), while p-STAT6 expression was significantly increased in atheromatous plaque (P < 0.01). The level of LC3-II was significantly higher in atheromatous plaque than that in fibrous plaque (P < 0.01). Macrophages in early atherosclerotic plaque were induced to M1 type through p-STAT1/NF-κB pathway and expressed moderate levels of autophagy; while macrophages in advanced plaques were induced to polarization of M2 type through p-STAT6 pathway. M2 macrophages expressed a higher level of autophagy than M1 macrophages.

Objective: To explore the effect of arteriosclerosis obliterans (ASO) blood stasis syndrome (BSS) serum on vascular endothelial cell injury and to study the regulation of Taohong Siwu Decoction (TSD) on it., Methods: Umbilical vein endothelial cell culture system was established. The serum endothelial cell injury model with ASO BSS was prepared. Low, medium, and high concentrations TSD containing serums were respectively added. The endothelial cell proliferation activity was observed by MTT method. Ultrastructures of endothelial cells were observed under transmission electron microscope. Changes of intracellular calcium ion concentration and the cytoskeleton were observed under laser confocal microscope. Contents of ET, NO, and transforming growth factor beta1 (TGF-beta1) in endothelial cell culture supernatant were detected by ELISA., Results: In ASO BSS serum group endothelial cell proliferation activities decreased, the cell structure was obviously destroyed, calcium ion concentration increased, contents of ET, NO and TGF-beta1 increased significantly (P < 0.01), and ET/NO ratio was imbalanced. After incubating with TSD drug containing serum, endothelial cell proliferation activities and injured cell structures were obviously improved; ET, NO and TGF-beta1 levels decreased (P < 0.05, P < 0.01), ET/NO ratios approximated to the normal level., Conclusion: The main mechanism of TSD for treating ASO ASS lied in improving injured vascular endothelial cells and endocrine disorder.

Objective: To discuss the effect of Taohong Siwu Decoction (TSD) in regulating functions of endothelial cells and treating arteriosclerosis obliterans (ASO)., Methods: The ASO model was prepared by using high-fat diet plus intimal injury. They were randomly divided into the model group (n = 10), the normal control group (n = 9), the low dose TSD group (group A, n = 12), the middle dose TSD group (group B, n = 10), and the high dose TSD group (group C, n = 9). Eight weeks after modeling, the limb blood perfusion was observed using laser Doppler flowmetry. The arterial morphology was observed using light microscope and transmission electron microscope. The number of circulating endothelial cells (CECs) was determined using Percoll density gradient centrifugation method. Serum levels of TNF-alpha, IL-1, ET-1, and NO were detected using double antibody sandwich assay of enzyme linked immunosorbent assay (ELISA)., Results: The ASO rat model was successfully established. Blood lipids levels significantly increased, the blood perfusion of left hind limbs significantly decreased, the number of CECs in the peripheral blood significantly increased, the arterial lumen was irregularly narrowed, the ultra-structure of vessel walls was damaged, serum levels of TNF-alpha, IL-1, and ET-1 significantly increased, and the serum level of NO significantly decreased in the model group, showing statistical difference when compared with the normal control group (P < 0.01). Compared with the model group, significant improvement in the aforesaid indices was shown in group B and C (P < 0.05, P < 0.01)., Conclusions: The injury and abnormal functions of endothelial cells is an important pathological process of ASO. As an effective recipe for treating ASO, TSD could protect vascular endothelial cells and improve the secretion function of vascular endothelial cells.

Aim: To observe the influence of tanshinone II A on the expression of toll like receptor 4(TLR4) and tumor necrosis factor-α(TNF-α) in cultured human umbilical veins endothelial cells EA.hy926 induced by LPS, and to investigate the molecular mechanism of tanshinone II A against atherosclerosis(AS)., Methods: The EA.hy926 cells were cultured in vitro. The mRNA and protein expression of TLR4 were tested by RT-PCR and immunocytochemistry technique respectively. The mRNA and protein expression of TNF-α were detected by RT-PCR and ELISA technique respectively., Results: The expression of TLR4 and TNF-α were both increased compared to normal group after stimulation of LPS(P<0.05). The expression of TLR4 and TNF-α in tanshinone II A group were obviously inhibited compared to stimulation group(P<0.05)., Conclusion: The molecular mechanism of tanshinone II A against AS is probably to inhibit the expression of TLR4 and TNF-α.