The objective of this study was to explain the physiological mechanisms through which Na_(2)SeO_(3) mitigates the growth and developmental inhibition of pakchoi under HgCl_(2)stress.The results showed that treatment w...The objective of this study was to explain the physiological mechanisms through which Na_(2)SeO_(3) mitigates the growth and developmental inhibition of pakchoi under HgCl_(2)stress.The results showed that treatment with HgCl_(2)(40 mg L^(−1))led to reduced biomass,dwarfing,root shortening,and root tip necrosis in pakchoi.Compared to control(CK),the activities of superoxide dismutase(SOD)and peroxidase(POD)in Hg treatment increased,and the content of malondialdehyde(MDA)also dramatically increased,which negatively impacted the growth of pakchoi.Low concentrations of Na_(2)SeO_(3)(0.2 mg L^(−1))significantly increased the content of soluble sugars compared with control,while chlorophyll,soluble proteins,free amino acids,and vitamin C had no significant changes.The results of the mixed treatments with HgCl_(2)and Na_(2)SeO_(3) suggested that selenium may be able to reduce the toxicity of mercury in pakchoi.The biomass,plant height,root length,chlorophyll content,soluble protein,other physiological indicators,and proline showed significant increases compared with the HgCl_(2)treatment.Additionally,the MDA content and mercury accumulation in pakchoi decreased.Our results revealed the antagonistic effects of selenium and mercury in pakchoi.Thus,a theoretical basis for studying pakchoi’s mercuryexcreted and selenium-rich cultivation technology was provided.展开更多
Sepsis is a life-threatening organ dysfunction caused by the dysregulated response of the host to an infection, and treatments are limited. Recently, a novel selenium source, selenium-enriched Cardamine violifolia(SEC...Sepsis is a life-threatening organ dysfunction caused by the dysregulated response of the host to an infection, and treatments are limited. Recently, a novel selenium source, selenium-enriched Cardamine violifolia(SEC) has attracted much attention due to its anti-inflammatory and antioxidant properties, but little is known about its role in the treatment of sepsis. Here, we found that SEC alleviated LPS-induced intestinal damage, as indicated by improved intestinal morphology, and increased disaccharidase activity and tight junction protein expression. Moreover, SEC ameliorated the LPS-induced release of pro-inflammatory cytokines, as indicated by decreased IL-6 level in the plasma and jejunum. Moreover, SEC improved intestinal antioxidant functions by regulating oxidative stress indicators and selenoproteins. In vitro, TNF-α-challenged IPEC-1 cells were examined and showed that selenium-enriched peptides, which are the main functional components extracted from Cardamine violifolia(CSP), increased cell viability, decreased lactate dehydrogenase activity and improved cell barrier function. Mechanistically, SEC ameliorated LPS/TNF-α-induced perturbations in mitochondrial dynamics in the jejunum and IPEC-1 cells. Moreover, CSPmediated cell barrier function is primarily dependent on the mitochondrial fusion protein MFN2 but not MFN1. Taken together,these results indicate that SEC mitigates sepsis-induced intestinal injury, which is associated with modulating mitochondrial fusion.展开更多
基金the Key Program of Hubei Province,Grant Number 2023BBA043.
文摘The objective of this study was to explain the physiological mechanisms through which Na_(2)SeO_(3) mitigates the growth and developmental inhibition of pakchoi under HgCl_(2)stress.The results showed that treatment with HgCl_(2)(40 mg L^(−1))led to reduced biomass,dwarfing,root shortening,and root tip necrosis in pakchoi.Compared to control(CK),the activities of superoxide dismutase(SOD)and peroxidase(POD)in Hg treatment increased,and the content of malondialdehyde(MDA)also dramatically increased,which negatively impacted the growth of pakchoi.Low concentrations of Na_(2)SeO_(3)(0.2 mg L^(−1))significantly increased the content of soluble sugars compared with control,while chlorophyll,soluble proteins,free amino acids,and vitamin C had no significant changes.The results of the mixed treatments with HgCl_(2)and Na_(2)SeO_(3) suggested that selenium may be able to reduce the toxicity of mercury in pakchoi.The biomass,plant height,root length,chlorophyll content,soluble protein,other physiological indicators,and proline showed significant increases compared with the HgCl_(2)treatment.Additionally,the MDA content and mercury accumulation in pakchoi decreased.Our results revealed the antagonistic effects of selenium and mercury in pakchoi.Thus,a theoretical basis for studying pakchoi’s mercuryexcreted and selenium-rich cultivation technology was provided.
基金supported by the National Natural Science Foundation of China (U22A20517, 32272906 and 32102566)the Project of Wuhan Science and Technology Bureau (2022020801010391)。
文摘Sepsis is a life-threatening organ dysfunction caused by the dysregulated response of the host to an infection, and treatments are limited. Recently, a novel selenium source, selenium-enriched Cardamine violifolia(SEC) has attracted much attention due to its anti-inflammatory and antioxidant properties, but little is known about its role in the treatment of sepsis. Here, we found that SEC alleviated LPS-induced intestinal damage, as indicated by improved intestinal morphology, and increased disaccharidase activity and tight junction protein expression. Moreover, SEC ameliorated the LPS-induced release of pro-inflammatory cytokines, as indicated by decreased IL-6 level in the plasma and jejunum. Moreover, SEC improved intestinal antioxidant functions by regulating oxidative stress indicators and selenoproteins. In vitro, TNF-α-challenged IPEC-1 cells were examined and showed that selenium-enriched peptides, which are the main functional components extracted from Cardamine violifolia(CSP), increased cell viability, decreased lactate dehydrogenase activity and improved cell barrier function. Mechanistically, SEC ameliorated LPS/TNF-α-induced perturbations in mitochondrial dynamics in the jejunum and IPEC-1 cells. Moreover, CSPmediated cell barrier function is primarily dependent on the mitochondrial fusion protein MFN2 but not MFN1. Taken together,these results indicate that SEC mitigates sepsis-induced intestinal injury, which is associated with modulating mitochondrial fusion.
