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We assessed the effects of EDTA and selected plant growth-promoting rhizobacteria (PGPR) on the phytoremediation of soils and sediments historically contaminated by Cr, Ni, and Cu. A total of 42 bacterial strains resistant to these heavy metals (HMs) were isolated and screened for PGP traits and metal bioaccumulation, and two Enterobacter spp. strains were finally selected. Phytoremediation pot experiments of 2 months duration were carried out with hemp (Cannabis sativa L.) and giant reed (Arundo donax L.) grown on soils and sediments respectively, comparing in both cases the effects of bioaugmentation with a single PGPR and EDTA addition on plant and root growth, plant HM uptake, HM leaching, as well as the changes that occurred in soil microbial communities (structure, biomass, and activity). Good removal percentages on a dry mass basis of Cr (0.4%), Ni (0.6%), and Cu (0.9%) were observed in giant reed while negligible values (<100‰) in hemp. In giant reed, HMs accumulated differentially in plant (rhizomes > > roots > leaves > stems) with largest quantities in rhizomes (Cr 0.6, Ni 3.7, and Cu 2.2 g plant–1). EDTA increased Ni and Cu translocation to aerial parts in both crops, despite that in sediments high HM concentrations in leachates were measured. PGPR did not impact fine root diameter distribution of both crops compared with control while EDTA negatively affected root diameter class length (DCL) distribution. Under HM contamination, giant reed roots become shorter (from 5.2 to 2.3 mm cm–3) while hemp roots become shorter and thickened from 0.13 to 0.26 mm. A consistent indirect effect of HM levels on the soil microbiome (diversity and activity) mediated by plant response (root DCL distribution) was observed. Multivariate analysis of bacterial diversity and activity revealed not only significant effects of plant and soil type (rhizosphere vs. bulk) but also a clear and similar differentiation of communities between control, EDTA, and PGPR treatments. We propose root DCL distribution as a key plant trait to understand detrimental effect of HMs on microbial communities. Positive evidence of the soil-microbe-plant interactions occurring when bioaugmentation with PGPR is associated with deep-rooting perennial crops makes this combination preferable over the one with chelating agents. Such knowledge might help to yield better bioaugmented bioremediation results in contaminated sites.

Major depressive disorder and major depressive episodes (MDD/MDE) are characterized by the activation of the immune–inflammatory response system (IRS) and the compensatory immune–regulatory system (CIRS). Cannabidiol (CBD) is a phytocannabinoid isolated from the cannabis plant, which is reported to have antidepressant-like and anti-inflammatory effects. The aim of the present study is to examine the effects of CBD on IRS, CIRS, M1, T helper (Th)-1, Th-2, Th-17, T regulatory (Treg) profiles, and growth factors in depression and healthy controls. Culture supernatant of stimulated (5 μg/mL of PHA and 25 μg/mL of LPS) whole blood of 30 depressed patients and 20 controls was assayed for cytokines using the LUMINEX assay. The effects of three CBD concentrations (0.1 µg/mL, 1 µg/mL, and 10 µg/mL) were examined. Depression was characterized by significantly increased PHA + LPS-stimulated Th-1, Th-2, Th-17, Treg, IRS, CIRS, and neurotoxicity profiles. CBD 0.1 µg/mL did not have any immune effects. CBD 1.0 µg/mL decreased CIRS activities but increased growth factor production, while CBD 10.0 µg/mL suppressed Th-1, Th-17, IRS, CIRS, and a neurotoxicity profile and enhanced T cell growth and growth factor production. CBD 1.0 to 10.0 µg/mL dose-dependently decreased sIL-1RA, IL-8, IL-9, IL-10, IL-13, CCL11, G-CSF, IFN-γ, CCL2, CCL4, and CCL5, and increased IL-1β, IL-4, IL-15, IL-17, GM-CSF, TNF-α, FGF, and VEGF. In summary, in this experiment, there was no beneficial effect of CBD on the activated immune profile of depression and higher CBD concentrations can worsen inflammatory processes.

Cannabidiol (CBD), the major nonpsychoactive Cannabis constituent, has been proposed for the treatment of a wide panel of neurological and neuropsychiatric disorders, including anxiety, schizophrenia, epilepsy and drug addiction due to the ability of its versatile scaffold to interact with diverse molecular targets that are not restricted to the endocannabinoid system. Albeit the molecular mechanisms responsible for the therapeutic effects of CBD have yet to be fully elucidated, many efforts have been devoted in the last decades to shed light on its complex pharmacological profile. In particular, an ever-increasing number of molecular targets linked to those disorders have been identified for this phytocannabinoid, along with the modulatory effects of CBD on their cascade signaling. In this view, here we will try to provide a comprehensive and up-to-date overview of the molecular basis underlying the therapeutic effects of CBD involved in the treatment of neurological and neuropsychiatric disorders.

为了探究叶面喷施外源水杨酸（Salicylic acid，SA）对小报春（Primula forbesii Franch.）镉（Cadmium，Cd）胁迫的缓解作用，本研究以小报春幼苗为试验材料，采用盆栽试验方法，在土壤Cd胁迫（150 mg·kg^-1）下，测定不同浓度（0，10，100，1 000 μmol·L^-1） SA处理下的小报春植株生长和生理特性指标。结果表明，低浓度SA （10，100 μmol·L^-1）能够使小报春株高、冠幅和地上部生物量增加，促进光合作用；低浓度SA能降低过氧化氢和丙二醛含量，提高超氧化物歧化酶（Superoxide dismutase，SOD）、过氧化物酶（Peroxidase，POD）和过氧化氢酶（Catalase，CAT）活性，促进可溶性糖和可溶性蛋白的产生；同时低浓度SA还能显著降低小报春幼苗叶片中的Cd含量，增加叶片中的钾和锌含量，降低钙和镁含量。而高浓度SA （1 000 μmol·L^-1）缓解作用下降，甚至对植株生长产生抑制作用。本研究表明，100 μmol·L^-1外源SA处理可以显著缓解150 mg·kg^-1土壤Cd胁迫对小报春幼苗的毒害作用，并降低植株镉积累。

为探究不同外源物质对Cd胁迫下绵毛水苏生理和生长的缓解效果,采用盆栽试验研究叶面喷施不同浓度水杨酸(SA)(0.5、1.0、1.5、2.0 mmol·L^-1)和谷胱甘肽(GSH)(0.1、0.2、0.3、0.4 mmol·L^-1) 对300 mg·kg^-1 Cd胁迫下绵毛水苏幼苗生长、渗透调节物质、抗氧化酶活性以及Cd含量等的影响。结果表明,外源SA和GSH改善了植物的叶色,提高了叶面积和萌蘖能力,并增加了地下、地上部干物质积累量。除0.4 mmol·L^-1 GSH处理第3天外,外源SA和GSH处理均提高了可溶性糖、可溶性蛋白和游离脯氨酸等渗透调节物质的含量,最高增幅分别为16.06%、14.13%、311.39%(SA)和50.28%、12.77%、313.77%(GSH);此外,SA和GSH分别使抗氧化酶(SOD、POD和CAT)活性最高增幅依次达57.39%、38.51%、26.81%和85.00%、60.77%、50.21%。绵毛水苏吸收的Cd主要累积在根部,外源SA对Cd吸收无明显影响,而GSH抑制了Cd向地上部的转运。综上可知,SA和GSH对Cd胁迫下的绵毛水苏均具有缓解作用,以1.5 mmol·L^-1 SA和0.3~0.4 mmol·L^-1 GSH效果较佳。本研究结果对绵毛水苏应用于Cd污染土壤植物修复具有重要意义。

The growth regulator, salicylic acid (SA) plays an important role in the induction of cell death in plants. Production of reactive oxygen species (ROS) by mitochondrial electron transport chain (mtETC), cytochrome c (cyt c) release from mitochondria and loss of mitochondrial integrity can be observed during cell death execution in plant tissues. The aim of this work was to study the putative role of hexokinases (HXKs) in the initiation of cell death using tomato (Solanum lycopersicum L.) leaves and mitochondria isolated from plants exposed to a sublethal, 0.1 mM and a cell death-inducing, 1 mM concentrations of SA. Both treatments enhanced ROS and nitric oxide (NO) production in the leaves, which contributed to a concentration-dependent loss of membrane integrity. Images prepared by transmission electron microscopy showed swelling and disorganisation of mitochondrial cristae and vacuolization of mitochondria after SA exposure. Using post-embedding immunohistochemistry, cyt c release from mitochondria was also detected after 1 mM SA treatment. Both SA treatments decreased the activity and transcript levels of HXKs in the leaves and the total mtHXK activity in the mitochondrial fraction. The role of mitochondrial hexokinases (mtHXKs) in ROS and NO production of isolated mitochondria was investigated by the addition of HXK substrate, glucose (Glc) and a specific HXK inhibitor, N-acetylglucosamine (NAG) to the mitochondrial suspension. Both SA treatments enhanced ROS production by mtETC in the presence of succinate and ADP, which was slightly inhibited by Glc and increased significantly by NAG in control and in 0.1 mM SA-treated mitochondria. These changes were not significant at 1 mM SA, which caused disorganisation of mitochondrial membranes. Thus the inhibition of mtHXK activity can contribute to the mitochondrial ROS production, but it is not involved in NO generation in SA-treated leaf mitochondria suggesting that SA can promote cell death by suppressing mtHXK transcription and activity.

In a previous study, we found that the combined addition of Al and Mn in the culture solution could alleviate the inhibition of barley growth by addition of Al or Mn alone. The current experiment was conducted in a greenhouse to investigate the physiological mechanisms of the antagonistic interaction using two barley genotypes, XZ16 (both Al and Mn tolerant) and ZU9 (both Al and Mn sensitive). The treatments consisted of three Al levels (0, 0.1, and 0.5 mM) and three Mn levels (0, 0.2, and 1.0 mM) and their combinations, and a completely randomized block design was used with three replications. The combined treatments had larger plant biomass, lower Al and Mn concentrations and accumulation in plant tissues, lower malondialdehyde content, and higher root ATPases activities, compared with Al or Mn alone treatment. The two genotypes had the similar trend in the antagonistic interaction, with ZU9 being more predominant than XZ16.

Wheat (Triticum aestivum L.) has relatively high tolerance to cadmium (Cd), but the underlying mechanisms are poorly understood. Growth and physiological parameters of wheat exposed to different Cd concentrations (0, 0.5, 5 and 50 µM) were characterized. The fresh weight, leaf chlorophyll and carotenoid concentrations and photosynthesis parameters did not differ among Cd treatments, suggesting relatively high Cd tolerance in wheat. However, the soluble sugar concentrations increased with the increasing Cd concentration and the soluble protein concentrations decreased in both shoots and roots, suggesting that the Cd application promoted nitrogen metabolism over carbon metabolism. In addition, the higher concentrations of MDA, GSH and AsA and activities of antioxidant enzymes (SOD, POD, and CAT) were observed in leaves and roots in the Cd50 treatment. Our results reveal that wheat can tolerate Cd by enhancing the antioxidant enzymes activities and increasing the concentration of ascorbate and glutathione.

Cardiovascular complications are the major cause of mortality in diabetic patients. However, the molecular mechanisms underlying diabetes-associated arrhythmias are unclear. We hypothesized that high glucose could adversely affect Na 1.5, the major cardiac sodium channel isoform of the heart, at least partially via oxidative stress. We further hypothesized that cannabidiol (CBD), one of the main constituents of Cannabis sativa, through its effects on Na 1.5, could protect against high glucose-elicited oxidative stress and cytotoxicity.To test these ideas, we used CHO cells transiently co-transfected with cDNA encoding human Na 1.5 α-subunit under control and high glucose conditions (50 or 100 mM for 24 hr). Several experimental and computational techniques were used, including voltage clamp of heterologous expression systems, cell viability assays, fluorescence assays and action potential modelling.High glucose evoked cell death associated with elevation in reactive oxygen species (ROS) right shifted the voltage dependence of conductance and steady-state fast inactivation, and increased persistent current leading to computational prolongation of action potential (hyperexcitability) which could result in long QT3 arrhythmia. CBD mitigated all the deleterious effects provoked by high glucose. Perfusion with lidocaine (a well-known sodium channel inhibitor with antioxidant effects) or co-incubation of Tempol (a well-known antioxidant) elicited protection, comparable to CBD, against the deleterious effects of high glucose.These findings suggest that, through its favourable antioxidant and sodium channel inhibitory effects, CBD may protect against high glucose-induced arrhythmia and cytotoxicity.© 2020 The British Pharmacological Society.