Islet beta cells(β-cells)produce insulin in response to high blood glucose levels,which is essential for preserving glucose homeostasis.Voltage-gated ion channels inβ-cells,including Na+,K+,and Ca2+channels,aid in t...Islet beta cells(β-cells)produce insulin in response to high blood glucose levels,which is essential for preserving glucose homeostasis.Voltage-gated ion channels inβ-cells,including Na+,K+,and Ca2+channels,aid in the release of insulin.The epithelial sodium channel alpha subunit(α-ENaC),a voltage-independent sodium ion channel,is also expressed in human pancreatic endocrine cells.However,there is no reported study on the function of ENaC in theβ-cells.In the current study,we found thatα-ENaC was expressed in human pancreatic glandule and pancreatic isletβ-cells.In the pancreas of db/db mice and high-fat diet-induced mice,and in mouse isletβ-cells(MIN6 cells)treated with palmitate,α-ENaC expression was increased.Whenα-ENaC was overexpressed in MIN6 cells,insulin content and glucose-induced insulin secretion were significantly reduced.On the other hand,palmitate injured isletβ-cells and suppressed insulin synthesis and secretion,but increasedα-ENaC expression in MIN6 cells.However,α-ENaC knockout(Scnn1a−/−)in MIN6 cells attenuatedβ-cell disorder induced by palmitate.Furthermore,α-ENaC regulated the ubiquitylation and degradation of sirtuin 2 inβ-cells.α-ENaC also modulatedβ-cell function in correlation with the inositol-requiring enzyme 1 alpha/X-box binding protein 1(IRE1α/XBP1)and protein kinase RNA-like endoplasmic reticulum kinase/C/EBP homologous protein(PERK/CHOP)endoplasmic reticulum stress pathways.These results suggest thatα-ENaC may play a novel role in insulin synthesis and secretion in theβ-cells,and the upregulation ofα-ENaC promotes isletβ-cell dysfunction.In conclusion,α-ENaC may be a key regulator involved in isletβ-cell damage and a potential therapeutic target for type 2 diabetes mellitus.展开更多
Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucid...Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucidated.Results In this study, we investigated the effects of hesperidin on H_(2)O_(2)-induced oxidative stress in b MECs and the underlying molecular mechanism. We found that hesperidin attenuated H_(2)O_(2)-induced cell damage by reducing reactive oxygen species(ROS) and malondialdehyde(MDA) levels, increasing catalase(CAT) activity, and improving cell proliferation and mitochondrial membrane potential. Moreover, hesperidin activated the Keap1/Nrf2/ARE signaling pathway by inducing the nuclear translocation of Nrf2 and the expression of its downstream genes NQO1 and HO-1, which are antioxidant enzymes involved in ROS scavenging and cellular redox balance. The protective effects of hesperidin were blocked by the Nrf2 inhibitor ML385, indicating that they were Nrf2 dependent.Conclusions Our results suggest that hesperidin could protect b MECs from oxidative stress injury by activating the Nrf2 signaling pathway, suggesting that hesperidin as a natural antioxidant has positive potential as a feed additive or plant drug to promote the health benefits of bovine mammary.展开更多
Abscisic acid(ABA),hydrogen peroxide(H_(2)O_(2)) and ascorbate(AsA)–glutathione(GSH)cycle are widely known for their participation in various stresses.However,the relationship between ABA and H_(2)O_(2) levels and th...Abscisic acid(ABA),hydrogen peroxide(H_(2)O_(2)) and ascorbate(AsA)–glutathione(GSH)cycle are widely known for their participation in various stresses.However,the relationship between ABA and H_(2)O_(2) levels and the AsA–GSH cycle under drought stress in wheat has not been studied.In this study,a hydroponic experiment was conducted in wheat seedlings subjected to 15%polyethylene glycol(PEG)6000–induced dehydration.Drought stress caused the rapid accumulation of endogenous ABA and H_(2)O_(2) and significantly decreased the number of root tips compared with the control.The application of ABA significantly increased the number of root tips,whereas the application of H_(2)O_(2) markedly reduced the number of root tips,compared with that under 15%PEG-6000.In addition,drought stress markedly increased the DHA,GSH and GSSG levels,but decreased the AsA levels,AsA/DHA and GSH/GSSG ratios compared with those in the control.The activities of the four enzymes in the AsA–GSH cycle were also markedly increased under drought stress,including glutathione reductase(GR),ascorbate peroxidase(APX),monodehydroascorbate reductase(MDHAR)and dehydroascorbate reductase(DHAR),compared with those in the control.However,the application of an ABA inhibitor significantly inhibited GR,DHAR and APX activities,whereas the application of an H_(2)O_(2) inhibitor significantly inhibited DHAR and MDHAR activities.Furthermore,the application of ABA inhibitor significantly promoted the increases of H_(2)O_(2) and the application of H_(2)O_(2) inhibitor significantly blocked the increases of ABA,compared with those under 15% PEG-6000.Taken together,the results indicated that ABA and H_(2)O_(2) probably interact under drought stress in wheat;and both of them can mediate drought stress by modulating the enzymes in AsA–GSH cycle,where ABA acts as the main regulator of GR,DHAR,and APX activities,and H_(2)O_(2) acts as the main regulator of DHAR and MDHAR activities.展开更多
Objective: To explore the protective effect of camellia oil against H2O2-induced oxidative stress injury in rat H9C2 cardiomyocytes. Methods: CCK8 method was used to detect the cell survival rate of H9C2 cardiomyocyte...Objective: To explore the protective effect of camellia oil against H2O2-induced oxidative stress injury in rat H9C2 cardiomyocytes. Methods: CCK8 method was used to detect the cell survival rate of H9C2 cardiomyocytes treated with different concentrations of H2O2. Normal cultured cells were used as the blank control group, and the cells were treated with 200 μmol/L H2O2 for 24 h. An oxidative stress injury model was constructed as the model group. The cells were pretreated with 1%, 0.1% and 0.01% camellia oil for 24 h, and then H2O2 was added for 24 h as the experimental group. The β-galactosidase senescence staining assay, mitochondrial membrane potential assay, EdU cell proliferation staining assay and scratch assay were used to observe the changes of cell senescence, mitochondrial membrane potential, proliferation, apoptosis and migration in each group. The superoxide dismutase (SOD) activity, lactate dehydrogenase (LDH) activity, and malondialdehyde (MDA) content of the cells in each group were detected by using the kit. Results: The cell viability of H9C2 cardiomyocytes treated with different concentrations of H2O2 was inhibited and positively correlated with the concentration of H2O2 (P<0.01). Compared with the blank control group, the positive rate of cell senescence, MDA content and LDH activity increased in the H2O2 model group (P<0.01);mitochondrial membrane potential, cellular value-added rate, migration rate and SOD activity decreased (P<0.01). Compared with the H2O2 model group, the positive rate of cellular senescence (P<0.01 or P<0.05), MDA content and LDH activity decreased (P< 0.01 or P<0.05);mitochondrial membrane potential increased, cell proliferation rate and migration rate increased (P<0.01 or P<0.05) in the experimental group. Conclusion: Camellia oil can significantly inhibit oxidative stress injury in H9C2 cells and exert cardiomyocyte protective effects.展开更多
Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of N...Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of Nitralia tangutorum Bobr. under salt stress were studied. N. tangutorum seedlings were subjected to 200 mmol·L^(-1) NaCl treatment with or without the exogenous application of H_(2)O_(2) for 7 days. The results showed that NaCl stress significantly increased the relative conductivity, the contents of thiobarbituric acid reactive substances(TBARS) and ROS(H_(2)O_(2) and O_(2)^(·-)), as well as promoted the activities of antioxidant enzymes including superoxide dismutase(SOD), peroxidase(POD), catalase(CAT), and ascorbate peroxidase(APX) in N. tangutorum leaves. In addition, exogenous H_(2)O_(2) decreased the relative conductivity, the contents of TBARS, H_(2)O_(2) and O_(2)^(·-), while further enhanced the activities of antioxidant enzymes. These results indicated that H_(2)O_(2) effectively alleviated the adverse effects of NaCl stress on N. tangutorum through the regulation of ROS metabolism.展开更多
BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal je...BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal jejunal bypass(DJB)surgery significantly improves brain glucose metabolism in T2DM rats,the role and the metabolism of DJB in improving brain oxidative stress and inflammation condition in T2DM rats remain unclear.AIM To investigate the role and metabolism of DJB in improving hypothalamic oxidative stress and inflammation condition in T2DM rats.METHODS A T2DM rat model was induced via a high-glucose and high-fat diet,combined with a low-dose streptozotocin injection.T2DM rats were divided into DJB operation and Sham operation groups.DJB surgical intervention was carried out on T2DM rats.The differential expression of hypothalamic proteins was analyzed using quantitative proteomics analysis.Proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of T2DM rats were analyzed by flow cytometry,quantitative real-time PCR,Western blotting,and immunofluorescence.RESULTS Quantitative proteomics analysis showed significant differences in proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of rats with T2DM-DJB after DJB surgery,compared to the T2DM-Sham groups of rats.Oxidative stress-related proteins(glucagon-like peptide 1 receptor,Nrf2,and HO-1)were significantly increased(P<0.05)in the hypothalamus of rats with T2DM after DJB surgery.DJB surgery significantly reduced(P<0.05)hypothalamic inflammation in T2DM rats by inhibiting the activation of NF-κB and decreasing the expression of interleukin(IL)-1βand IL-6.DJB surgery significantly reduced(P<0.05)the expression of factors related to neuronal injury(glial fibrillary acidic protein and Caspase-3)in the hypothalamus of T2DM rats and upregulated(P<0.05)the expression of neuroprotective factors(C-fos,Ki67,Bcl-2,and BDNF),thereby reducing hypothalamic injury in T2DM rats.CONCLUSION DJB surgery improve oxidative stress and inflammation in the hypothalamus of T2DM rats and reduce neuronal cell injury by activating the glucagon-like peptide 1 receptor-mediated Nrf2/HO-1 signaling pathway.展开更多
Osmotic stress caused by low-temperature,drought and salinity was a prevalent abiotic stress in plant that severely inhibited plant development and agricultural yield,particularly in tea plant.Jasmonic acid(JA)is an i...Osmotic stress caused by low-temperature,drought and salinity was a prevalent abiotic stress in plant that severely inhibited plant development and agricultural yield,particularly in tea plant.Jasmonic acid(JA)is an important phytohormone involving in plant stress.However,underlying molecular mechanisms of JA modulated osmotic stress response remains unclear.In this study,high concentration of mannitol induced JA accumulation and increase of peroxidase activity in tea plant.Integrated transcriptome mined a JA signaling master,MYC2 transcription factor is shown as a hub regulator that induced by mannitol,expression of which positively correlated with JA biosynthetic genes(LOX and AOS)and peroxidase genes(PER).CsMYC2 was determined as a nuclei-localized transcription activator,furthermore,ProteinDNA interaction analysis indicated that CsMYC2 was positive regulator that activated the transcription of CsLOX7,CsAOS2,CsPER1 and CsPER3via bound with their promoters,respectively.Suppression of CsMYC2 expression resulted in a reduced JA content and peroxidase activity and osmotic stress tolerance of tea plant.Overexpression of CsMYC2 in Arabidopsis improved JA content,peroxidase activity and plants tolerance against mannitol stress.Together,we proposed a positive feedback loop mediated by CsMYC2,CsLOX7 and CsAOS2 which constituted to increase the tolerance of osmotic stress through fine-tuning the accumulation of JA levels and increase of POD activity in tea plant.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos.81870467 and 82270717 to XL,and 81970673 to FC)China Postdoctoral Science Foundation(Grant No.2023M731630 to XZhang)Postgraduate Research and Practice Innovation Program of Jiangsu Province(Grant No.KYCX21_1588 to XZhou).
文摘Islet beta cells(β-cells)produce insulin in response to high blood glucose levels,which is essential for preserving glucose homeostasis.Voltage-gated ion channels inβ-cells,including Na+,K+,and Ca2+channels,aid in the release of insulin.The epithelial sodium channel alpha subunit(α-ENaC),a voltage-independent sodium ion channel,is also expressed in human pancreatic endocrine cells.However,there is no reported study on the function of ENaC in theβ-cells.In the current study,we found thatα-ENaC was expressed in human pancreatic glandule and pancreatic isletβ-cells.In the pancreas of db/db mice and high-fat diet-induced mice,and in mouse isletβ-cells(MIN6 cells)treated with palmitate,α-ENaC expression was increased.Whenα-ENaC was overexpressed in MIN6 cells,insulin content and glucose-induced insulin secretion were significantly reduced.On the other hand,palmitate injured isletβ-cells and suppressed insulin synthesis and secretion,but increasedα-ENaC expression in MIN6 cells.However,α-ENaC knockout(Scnn1a−/−)in MIN6 cells attenuatedβ-cell disorder induced by palmitate.Furthermore,α-ENaC regulated the ubiquitylation and degradation of sirtuin 2 inβ-cells.α-ENaC also modulatedβ-cell function in correlation with the inositol-requiring enzyme 1 alpha/X-box binding protein 1(IRE1α/XBP1)and protein kinase RNA-like endoplasmic reticulum kinase/C/EBP homologous protein(PERK/CHOP)endoplasmic reticulum stress pathways.These results suggest thatα-ENaC may play a novel role in insulin synthesis and secretion in theβ-cells,and the upregulation ofα-ENaC promotes isletβ-cell dysfunction.In conclusion,α-ENaC may be a key regulator involved in isletβ-cell damage and a potential therapeutic target for type 2 diabetes mellitus.
基金supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (Grant No. XDA26040304)。
文摘Background Hesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells(b MECs) exposed to oxidative stress have not been elucidated.Results In this study, we investigated the effects of hesperidin on H_(2)O_(2)-induced oxidative stress in b MECs and the underlying molecular mechanism. We found that hesperidin attenuated H_(2)O_(2)-induced cell damage by reducing reactive oxygen species(ROS) and malondialdehyde(MDA) levels, increasing catalase(CAT) activity, and improving cell proliferation and mitochondrial membrane potential. Moreover, hesperidin activated the Keap1/Nrf2/ARE signaling pathway by inducing the nuclear translocation of Nrf2 and the expression of its downstream genes NQO1 and HO-1, which are antioxidant enzymes involved in ROS scavenging and cellular redox balance. The protective effects of hesperidin were blocked by the Nrf2 inhibitor ML385, indicating that they were Nrf2 dependent.Conclusions Our results suggest that hesperidin could protect b MECs from oxidative stress injury by activating the Nrf2 signaling pathway, suggesting that hesperidin as a natural antioxidant has positive potential as a feed additive or plant drug to promote the health benefits of bovine mammary.
基金This research was funded by the National Key Research and Development Program of China(2023YFD2301505).
文摘Abscisic acid(ABA),hydrogen peroxide(H_(2)O_(2)) and ascorbate(AsA)–glutathione(GSH)cycle are widely known for their participation in various stresses.However,the relationship between ABA and H_(2)O_(2) levels and the AsA–GSH cycle under drought stress in wheat has not been studied.In this study,a hydroponic experiment was conducted in wheat seedlings subjected to 15%polyethylene glycol(PEG)6000–induced dehydration.Drought stress caused the rapid accumulation of endogenous ABA and H_(2)O_(2) and significantly decreased the number of root tips compared with the control.The application of ABA significantly increased the number of root tips,whereas the application of H_(2)O_(2) markedly reduced the number of root tips,compared with that under 15%PEG-6000.In addition,drought stress markedly increased the DHA,GSH and GSSG levels,but decreased the AsA levels,AsA/DHA and GSH/GSSG ratios compared with those in the control.The activities of the four enzymes in the AsA–GSH cycle were also markedly increased under drought stress,including glutathione reductase(GR),ascorbate peroxidase(APX),monodehydroascorbate reductase(MDHAR)and dehydroascorbate reductase(DHAR),compared with those in the control.However,the application of an ABA inhibitor significantly inhibited GR,DHAR and APX activities,whereas the application of an H_(2)O_(2) inhibitor significantly inhibited DHAR and MDHAR activities.Furthermore,the application of ABA inhibitor significantly promoted the increases of H_(2)O_(2) and the application of H_(2)O_(2) inhibitor significantly blocked the increases of ABA,compared with those under 15% PEG-6000.Taken together,the results indicated that ABA and H_(2)O_(2) probably interact under drought stress in wheat;and both of them can mediate drought stress by modulating the enzymes in AsA–GSH cycle,where ABA acts as the main regulator of GR,DHAR,and APX activities,and H_(2)O_(2) acts as the main regulator of DHAR and MDHAR activities.
基金National Natural Science Foundation of China(No.82160597)Guangxi Natural Science Foundation Project(No.2020GXNSFAA159148)。
文摘Objective: To explore the protective effect of camellia oil against H2O2-induced oxidative stress injury in rat H9C2 cardiomyocytes. Methods: CCK8 method was used to detect the cell survival rate of H9C2 cardiomyocytes treated with different concentrations of H2O2. Normal cultured cells were used as the blank control group, and the cells were treated with 200 μmol/L H2O2 for 24 h. An oxidative stress injury model was constructed as the model group. The cells were pretreated with 1%, 0.1% and 0.01% camellia oil for 24 h, and then H2O2 was added for 24 h as the experimental group. The β-galactosidase senescence staining assay, mitochondrial membrane potential assay, EdU cell proliferation staining assay and scratch assay were used to observe the changes of cell senescence, mitochondrial membrane potential, proliferation, apoptosis and migration in each group. The superoxide dismutase (SOD) activity, lactate dehydrogenase (LDH) activity, and malondialdehyde (MDA) content of the cells in each group were detected by using the kit. Results: The cell viability of H9C2 cardiomyocytes treated with different concentrations of H2O2 was inhibited and positively correlated with the concentration of H2O2 (P<0.01). Compared with the blank control group, the positive rate of cell senescence, MDA content and LDH activity increased in the H2O2 model group (P<0.01);mitochondrial membrane potential, cellular value-added rate, migration rate and SOD activity decreased (P<0.01). Compared with the H2O2 model group, the positive rate of cellular senescence (P<0.01 or P<0.05), MDA content and LDH activity decreased (P< 0.01 or P<0.05);mitochondrial membrane potential increased, cell proliferation rate and migration rate increased (P<0.01 or P<0.05) in the experimental group. Conclusion: Camellia oil can significantly inhibit oxidative stress injury in H9C2 cells and exert cardiomyocyte protective effects.
基金Supported by the Natural Science Foundation of Heilongjiang Province(LH2019C021)。
文摘Salt stress is a major abiotic stress limiting plant growth and yield. In the present study, the effects of exogenous H_(2)O_(2) on the reactive oxygen species(ROS) metabolism and the antioxidant system in leaves of Nitralia tangutorum Bobr. under salt stress were studied. N. tangutorum seedlings were subjected to 200 mmol·L^(-1) NaCl treatment with or without the exogenous application of H_(2)O_(2) for 7 days. The results showed that NaCl stress significantly increased the relative conductivity, the contents of thiobarbituric acid reactive substances(TBARS) and ROS(H_(2)O_(2) and O_(2)^(·-)), as well as promoted the activities of antioxidant enzymes including superoxide dismutase(SOD), peroxidase(POD), catalase(CAT), and ascorbate peroxidase(APX) in N. tangutorum leaves. In addition, exogenous H_(2)O_(2) decreased the relative conductivity, the contents of TBARS, H_(2)O_(2) and O_(2)^(·-), while further enhanced the activities of antioxidant enzymes. These results indicated that H_(2)O_(2) effectively alleviated the adverse effects of NaCl stress on N. tangutorum through the regulation of ROS metabolism.
基金Supported by the Natural Science Foundation of China,No.82070856the Science and Technology Development Plan of Shandong Medical and Health Science,No.202102040075+1 种基金Scientific Research Plan of Weifang Health Commission,No.WFWSJK-2022-010 and No.WFWSJK-2022-008Weifang Science and Technology Development Plan,No.2021YX071 and No.2021YX070.
文摘BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal jejunal bypass(DJB)surgery significantly improves brain glucose metabolism in T2DM rats,the role and the metabolism of DJB in improving brain oxidative stress and inflammation condition in T2DM rats remain unclear.AIM To investigate the role and metabolism of DJB in improving hypothalamic oxidative stress and inflammation condition in T2DM rats.METHODS A T2DM rat model was induced via a high-glucose and high-fat diet,combined with a low-dose streptozotocin injection.T2DM rats were divided into DJB operation and Sham operation groups.DJB surgical intervention was carried out on T2DM rats.The differential expression of hypothalamic proteins was analyzed using quantitative proteomics analysis.Proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of T2DM rats were analyzed by flow cytometry,quantitative real-time PCR,Western blotting,and immunofluorescence.RESULTS Quantitative proteomics analysis showed significant differences in proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of rats with T2DM-DJB after DJB surgery,compared to the T2DM-Sham groups of rats.Oxidative stress-related proteins(glucagon-like peptide 1 receptor,Nrf2,and HO-1)were significantly increased(P<0.05)in the hypothalamus of rats with T2DM after DJB surgery.DJB surgery significantly reduced(P<0.05)hypothalamic inflammation in T2DM rats by inhibiting the activation of NF-κB and decreasing the expression of interleukin(IL)-1βand IL-6.DJB surgery significantly reduced(P<0.05)the expression of factors related to neuronal injury(glial fibrillary acidic protein and Caspase-3)in the hypothalamus of T2DM rats and upregulated(P<0.05)the expression of neuroprotective factors(C-fos,Ki67,Bcl-2,and BDNF),thereby reducing hypothalamic injury in T2DM rats.CONCLUSION DJB surgery improve oxidative stress and inflammation in the hypothalamus of T2DM rats and reduce neuronal cell injury by activating the glucagon-like peptide 1 receptor-mediated Nrf2/HO-1 signaling pathway.
基金supported by the National Natural Science Foundation of China(Grant Nos.32202542 and U20A2045)the Project of Major Science and Technology in Anhui Province(Grant No.202003a06020021)+2 种基金the Project of Science and Technology of Yunnan Province(Grant No.202102AE090038)Anhui Provincial Natural Science Foundation(Grant No.2108085QC121)the Natural Science Projects for Colleges and Universities in the Anhui Province(Grant No.KJ2021A0145)。
文摘Osmotic stress caused by low-temperature,drought and salinity was a prevalent abiotic stress in plant that severely inhibited plant development and agricultural yield,particularly in tea plant.Jasmonic acid(JA)is an important phytohormone involving in plant stress.However,underlying molecular mechanisms of JA modulated osmotic stress response remains unclear.In this study,high concentration of mannitol induced JA accumulation and increase of peroxidase activity in tea plant.Integrated transcriptome mined a JA signaling master,MYC2 transcription factor is shown as a hub regulator that induced by mannitol,expression of which positively correlated with JA biosynthetic genes(LOX and AOS)and peroxidase genes(PER).CsMYC2 was determined as a nuclei-localized transcription activator,furthermore,ProteinDNA interaction analysis indicated that CsMYC2 was positive regulator that activated the transcription of CsLOX7,CsAOS2,CsPER1 and CsPER3via bound with their promoters,respectively.Suppression of CsMYC2 expression resulted in a reduced JA content and peroxidase activity and osmotic stress tolerance of tea plant.Overexpression of CsMYC2 in Arabidopsis improved JA content,peroxidase activity and plants tolerance against mannitol stress.Together,we proposed a positive feedback loop mediated by CsMYC2,CsLOX7 and CsAOS2 which constituted to increase the tolerance of osmotic stress through fine-tuning the accumulation of JA levels and increase of POD activity in tea plant.