Hesperetin ameliorates diabetes-associated anxiety and depression-like behaviors in rats via activating Nrf2/ARE pathway
Diabetes-associated affective disorders are of wide concern, and oxidative stress plays a vital role in the pathological process. This study was to investigate the cerebroprotective effects of hesperetin against anxious and depressive disorders caused by diabetes, exploring the potential mechanisms...
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| Veröffentlicht in: | Metabolic brain disease 2021-10, Vol.36 (7), p.1969-1983 |
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| container_end_page | 1983 |
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| container_issue | 7 |
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| container_title | Metabolic brain disease |
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| creator | Zhu, Xia Zhang, Yu-Meng Zhang, Meng-Ya Chen, Ya-Jing Liu, Yao-Wu |
| description | Diabetes-associated affective disorders are of wide concern, and oxidative stress plays a vital role in the pathological process. This study was to investigate the cerebroprotective effects of hesperetin against anxious and depressive disorders caused by diabetes, exploring the potential mechanisms related to activation of Nrf2/ARE pathway. Streptozotocin-induced diabetic rats were intragastrically administrated with hesperetin (0, 50, and 150 mg/kg) for 10 weeks. Forced swimming test, open field test, and elevated plus maze were used to evaluate the anxiety and depression-like behaviors of rats. The brain was collected for assays of Nrf2/ARE pathway. Moreover, high glucose-cultured SH-SY5Y cells were used to further examine the neuroprotective effects of hesperetin and underlying mechanisms. Hesperetin showed anxiolytic and antidepressant effects in diabetic rats according to the behavior tests, and increased p-Nrf2 in cytoplasm and Nrf2 in nucleus followed by elevations in mRNA levels and protein expression of glyoxalase 1 (Glo-1) and γ-glutamylcysteine synthetase (γ-GCS) in brain, known target genes of Nrf2/ARE signaling. Moreover, hesperetin attenuated high glucose-induced neuronal damages through activation of the classical Nrf2/ARE pathway in SH-SY5Y cells. Further study indicated that PKC inhibition or GSK-3β activation pretreatment attenuated even abolished the effect of hesperetin on the protein expression of Glo-1 and γ-GCS in high glucose-cultured SH-SY5Y cells. In summary, hesperetin ameliorated diabetes-associated anxiety and depression-like behaviors in rats, which was achieved through activation of the Nrf2/ARE pathway. Furthermore, an increase in nuclear Nrf2 phosphorylation from PKC activation and GSK-3β inhibition contributed to the activation of Nrf2/ARE pathway by hesperetin. |
| doi_str_mv | 10.1007/s11011-021-00785-6 |
| format | Article |
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This study was to investigate the cerebroprotective effects of hesperetin against anxious and depressive disorders caused by diabetes, exploring the potential mechanisms related to activation of Nrf2/ARE pathway. Streptozotocin-induced diabetic rats were intragastrically administrated with hesperetin (0, 50, and 150 mg/kg) for 10 weeks. Forced swimming test, open field test, and elevated plus maze were used to evaluate the anxiety and depression-like behaviors of rats. The brain was collected for assays of Nrf2/ARE pathway. Moreover, high glucose-cultured SH-SY5Y cells were used to further examine the neuroprotective effects of hesperetin and underlying mechanisms. Hesperetin showed anxiolytic and antidepressant effects in diabetic rats according to the behavior tests, and increased p-Nrf2 in cytoplasm and Nrf2 in nucleus followed by elevations in mRNA levels and protein expression of glyoxalase 1 (Glo-1) and γ-glutamylcysteine synthetase (γ-GCS) in brain, known target genes of Nrf2/ARE signaling. Moreover, hesperetin attenuated high glucose-induced neuronal damages through activation of the classical Nrf2/ARE pathway in SH-SY5Y cells. Further study indicated that PKC inhibition or GSK-3β activation pretreatment attenuated even abolished the effect of hesperetin on the protein expression of Glo-1 and γ-GCS in high glucose-cultured SH-SY5Y cells. In summary, hesperetin ameliorated diabetes-associated anxiety and depression-like behaviors in rats, which was achieved through activation of the Nrf2/ARE pathway. Furthermore, an increase in nuclear Nrf2 phosphorylation from PKC activation and GSK-3β inhibition contributed to the activation of Nrf2/ARE pathway by hesperetin.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-021-00785-6</identifier><identifier>PMID: 34273043</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Affective disorders ; Animals ; Antidepressants ; Anxiety ; Anxiety - drug therapy ; Anxiety - etiology ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Cytoplasm ; Depression - drug therapy ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Field tests ; Gene expression ; Glucose ; Glycogen Synthase Kinase 3 beta - metabolism ; Hesperidin ; Mental depression ; Mental disorders ; Metabolic Diseases ; mRNA ; Neurology ; Neuroprotection ; Neurosciences ; NF-E2-Related Factor 2 - metabolism ; Oncology ; Open-field behavior ; Original Article ; Oxidative Stress ; Phosphorylation ; Protein expression ; Protein kinase C ; Proteins ; Rats ; Rodents ; Streptozocin ; γ-Glutamylcysteine</subject><ispartof>Metabolic brain disease, 2021-10, Vol.36 (7), p.1969-1983</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. 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This study was to investigate the cerebroprotective effects of hesperetin against anxious and depressive disorders caused by diabetes, exploring the potential mechanisms related to activation of Nrf2/ARE pathway. Streptozotocin-induced diabetic rats were intragastrically administrated with hesperetin (0, 50, and 150 mg/kg) for 10 weeks. Forced swimming test, open field test, and elevated plus maze were used to evaluate the anxiety and depression-like behaviors of rats. The brain was collected for assays of Nrf2/ARE pathway. Moreover, high glucose-cultured SH-SY5Y cells were used to further examine the neuroprotective effects of hesperetin and underlying mechanisms. Hesperetin showed anxiolytic and antidepressant effects in diabetic rats according to the behavior tests, and increased p-Nrf2 in cytoplasm and Nrf2 in nucleus followed by elevations in mRNA levels and protein expression of glyoxalase 1 (Glo-1) and γ-glutamylcysteine synthetase (γ-GCS) in brain, known target genes of Nrf2/ARE signaling. Moreover, hesperetin attenuated high glucose-induced neuronal damages through activation of the classical Nrf2/ARE pathway in SH-SY5Y cells. Further study indicated that PKC inhibition or GSK-3β activation pretreatment attenuated even abolished the effect of hesperetin on the protein expression of Glo-1 and γ-GCS in high glucose-cultured SH-SY5Y cells. In summary, hesperetin ameliorated diabetes-associated anxiety and depression-like behaviors in rats, which was achieved through activation of the Nrf2/ARE pathway. Furthermore, an increase in nuclear Nrf2 phosphorylation from PKC activation and GSK-3β inhibition contributed to the activation of Nrf2/ARE pathway by hesperetin.</description><subject>Affective disorders</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Anxiety</subject><subject>Anxiety - drug therapy</subject><subject>Anxiety - etiology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Cytoplasm</subject><subject>Depression - drug therapy</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Field tests</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Hesperidin</subject><subject>Mental depression</subject><subject>Mental disorders</subject><subject>Metabolic Diseases</subject><subject>mRNA</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oncology</subject><subject>Open-field behavior</subject><subject>Original Article</subject><subject>Oxidative Stress</subject><subject>Phosphorylation</subject><subject>Protein expression</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Streptozocin</subject><subject>γ-Glutamylcysteine</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU9v1DAQxS0EotvCF-CALHHhEur_iY9VVVqkCqSqPVtOPGldsknwZJfut2faLSBx4GCNNfPez9Y8xt5J8UkKUR-jlELKSig6om5s5V6wlbS1rmrt7Eu2Eg01a-PFATtEvBdCaCv9a3agjaq1MHrFHi4AZyiw5JHHNQx5KnEB5CnHFuhSRcSpy9RLPI4PGZYd1cQTzAUQ8zRWQ_4OvIW7uCUzcgIRAvk2Rx67JW8jsW_519Kr45OrMz7H5e5n3L1hr_o4ILx9rkfs5vPZ9elFdfnt_MvpyWXVGSOXqu9k8l57BaozNjkvo3A1GN973yrZJQdWxyaqXijjGmGdcKk32rWyoYHQR-zjnjuX6ccGcAnrjB0MQxxh2mBQ1irvaTOepB_-kd5PmzLS70hVK1qxko9AtVd1ZUIs0Ie55HUsuyBFeMwl7HMJlEt4yiU4Mr1_Rm_aNaQ_lt9BkEDvBUij8RbK37f_g_0FBEuYig</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>Zhu, Xia</creator><creator>Zhang, Yu-Meng</creator><creator>Zhang, Meng-Ya</creator><creator>Chen, Ya-Jing</creator><creator>Liu, Yao-Wu</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20211001</creationdate><title>Hesperetin ameliorates diabetes-associated anxiety and depression-like behaviors in rats via activating Nrf2/ARE pathway</title><author>Zhu, Xia ; 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This study was to investigate the cerebroprotective effects of hesperetin against anxious and depressive disorders caused by diabetes, exploring the potential mechanisms related to activation of Nrf2/ARE pathway. Streptozotocin-induced diabetic rats were intragastrically administrated with hesperetin (0, 50, and 150 mg/kg) for 10 weeks. Forced swimming test, open field test, and elevated plus maze were used to evaluate the anxiety and depression-like behaviors of rats. The brain was collected for assays of Nrf2/ARE pathway. Moreover, high glucose-cultured SH-SY5Y cells were used to further examine the neuroprotective effects of hesperetin and underlying mechanisms. Hesperetin showed anxiolytic and antidepressant effects in diabetic rats according to the behavior tests, and increased p-Nrf2 in cytoplasm and Nrf2 in nucleus followed by elevations in mRNA levels and protein expression of glyoxalase 1 (Glo-1) and γ-glutamylcysteine synthetase (γ-GCS) in brain, known target genes of Nrf2/ARE signaling. Moreover, hesperetin attenuated high glucose-induced neuronal damages through activation of the classical Nrf2/ARE pathway in SH-SY5Y cells. Further study indicated that PKC inhibition or GSK-3β activation pretreatment attenuated even abolished the effect of hesperetin on the protein expression of Glo-1 and γ-GCS in high glucose-cultured SH-SY5Y cells. In summary, hesperetin ameliorated diabetes-associated anxiety and depression-like behaviors in rats, which was achieved through activation of the Nrf2/ARE pathway. Furthermore, an increase in nuclear Nrf2 phosphorylation from PKC activation and GSK-3β inhibition contributed to the activation of Nrf2/ARE pathway by hesperetin.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34273043</pmid><doi>10.1007/s11011-021-00785-6</doi><tpages>15</tpages></addata></record> |
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| subjects | Affective disorders Animals Antidepressants Anxiety Anxiety - drug therapy Anxiety - etiology Biochemistry Biomedical and Life Sciences Biomedicine Brain Cytoplasm Depression - drug therapy Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Field tests Gene expression Glucose Glycogen Synthase Kinase 3 beta - metabolism Hesperidin Mental depression Mental disorders Metabolic Diseases mRNA Neurology Neuroprotection Neurosciences NF-E2-Related Factor 2 - metabolism Oncology Open-field behavior Original Article Oxidative Stress Phosphorylation Protein expression Protein kinase C Proteins Rats Rodents Streptozocin γ-Glutamylcysteine |
| title | Hesperetin ameliorates diabetes-associated anxiety and depression-like behaviors in rats via activating Nrf2/ARE pathway |
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