Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway
Hua Li,1,* Limei Lv,2,* Chunyan Wu,3 Jisheng Qi,4 Baolin Shi5 1Department of Neurology, Anqiu People’s Hospital, Anqiu 262100, Shandong, People’s Republic of China; 2Department of Neurology, Traditional Chinese Medical Hospital of Anqiu, Anqiu 262100, People’s Republic...
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Dove Medical Press
2020
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oai:doaj.org-article:74bfff96ebf04aaab512690a9f1684962021-12-02T08:36:24ZMethyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway1178-2021https://doaj.org/article/74bfff96ebf04aaab512690a9f1684962020-06-01T00:00:00Zhttps://www.dovepress.com/methyl-jasmonate-protects-microglial-cells-against-beta-amyloid-induce-peer-reviewed-article-NDThttps://doaj.org/toc/1178-2021Hua Li,1,* Limei Lv,2,* Chunyan Wu,3 Jisheng Qi,4 Baolin Shi5 1Department of Neurology, Anqiu People’s Hospital, Anqiu 262100, Shandong, People’s Republic of China; 2Department of Neurology, Traditional Chinese Medical Hospital of Anqiu, Anqiu 262100, People’s Republic of China; 3Department of Neurology, Affiliated Hospital of Weifang Medical College, Weifang 261031, Shandong, People’s Republic of China; 4Department of Rehabilitation Medicine, Shandong Rongjun General Hospital, Jinan 250000, Shandong, People’s Republic of China; 5Department of Neurology, Weifang People’s Hospital, Weifang 261031, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Baolin ShiDepartment of Neurology, Weifang People’s Hospital, No. 151 Guangwen Street, Kuiwen District, Weifang 261031, Shandong, People’s Republic of ChinaTel +86-15965096500Email cengbohuan58112@163.comBackground: β-Amyloid (Aβ) induces oxidative stress and inflammation of microglial cells, thus leading to Alzheimer’s disease. Methyl jasmonate (MeJA) is reported to have anti-inflammatory and anti-oxidant effects. However, the potential roles of MeJA in Aβ-induced cell activities and the underlying mechanism are unclear.Methods: Microglial cell line BV-2 was stimulated by 20 μM Aβ and/or 20 μM MeJA and then divided into four groups (control, Aβ, MeJA, and Aβ+MeJA). Cell viability was detected by MTT assay. MDA, SOD activity, and ROS were detected by fluorescence spectrophotometry and immunofluorescence assay. Nrf2 and HO-1 were detected by qRT-PCR and Western blot. Furthermore, inflammatory cytokines (p-NFκB, TLR4, TNF-α, IL-1β, and IL-6) and apoptosis factors (Bcl-2, Bax, and cl-casp-3) were detected by Western blot. TUNEL assay was applied to investigate apoptosis rate. Moreover, the mechanism of how MeJA played anti-oxidative stress and anti-inflammatory roles was investigated by silencing of Nrf2 via siRNA.Results: The result of MTT assay showed that MeJA improved the decreased viability of BV-2 cells induced by Aβ. The detection of MDA, SOD activity, and ROS showed the oxidative stress levels were decreased in Aβ+MeJA group compared with Aβ group. Nrf2, HO-1, and SOD were significantly up-regulated in Aβ+MeJA group compared with Aβ group (p< 0.01). In contrast, inflammatory cytokines were significantly down-regulated in Aβ+MeJA group compared with Aβ group (p< 0.05). Similarly, the expressions of apoptosis cytokines and TUNEL assay suggested a decreased apoptosis rate in Aβ+MeJA group compared to Aβ group (p< 0.01). Finally, results of Nrf2 knockdown experiment showed down-regulations of anti-oxidative stress factors (Nrf2, HO-1 and SOD), up-regulations of inflammatory cytokines, and increased ratio of Bax to Bcl in Aβ+MeJA+si-Nrf2 group compared with Aβ+MeJA group (p< 0.01).Conclusion: MeJA could relieve Aβ-induced oxidative stress and inflammatory response in microglial cells by activating Nrf2/HO-1 pathway.Keywords: methyl jasmonate, Nrf2-dependent HO-1 pathway, β-amyloid, oxidative stress, inflammatory cytokinesLi HLv LWu CQi JShi BDove Medical Pressarticlemethyl jasmonatenrf2-dependent ho-1 pathwayβ-amyloidoxidative stressinflammatory cytokines.Neurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol Volume 16, Pp 1399-1410 (2020) |
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DOAJ |
| collection |
DOAJ |
| language |
EN |
| topic |
methyl jasmonate nrf2-dependent ho-1 pathway β-amyloid oxidative stress inflammatory cytokines. Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 |
| spellingShingle |
methyl jasmonate nrf2-dependent ho-1 pathway β-amyloid oxidative stress inflammatory cytokines. Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Li H Lv L Wu C Qi J Shi B Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway |
| description |
Hua Li,1,* Limei Lv,2,* Chunyan Wu,3 Jisheng Qi,4 Baolin Shi5 1Department of Neurology, Anqiu People’s Hospital, Anqiu 262100, Shandong, People’s Republic of China; 2Department of Neurology, Traditional Chinese Medical Hospital of Anqiu, Anqiu 262100, People’s Republic of China; 3Department of Neurology, Affiliated Hospital of Weifang Medical College, Weifang 261031, Shandong, People’s Republic of China; 4Department of Rehabilitation Medicine, Shandong Rongjun General Hospital, Jinan 250000, Shandong, People’s Republic of China; 5Department of Neurology, Weifang People’s Hospital, Weifang 261031, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Baolin ShiDepartment of Neurology, Weifang People’s Hospital, No. 151 Guangwen Street, Kuiwen District, Weifang 261031, Shandong, People’s Republic of ChinaTel +86-15965096500Email cengbohuan58112@163.comBackground: β-Amyloid (Aβ) induces oxidative stress and inflammation of microglial cells, thus leading to Alzheimer’s disease. Methyl jasmonate (MeJA) is reported to have anti-inflammatory and anti-oxidant effects. However, the potential roles of MeJA in Aβ-induced cell activities and the underlying mechanism are unclear.Methods: Microglial cell line BV-2 was stimulated by 20 μM Aβ and/or 20 μM MeJA and then divided into four groups (control, Aβ, MeJA, and Aβ+MeJA). Cell viability was detected by MTT assay. MDA, SOD activity, and ROS were detected by fluorescence spectrophotometry and immunofluorescence assay. Nrf2 and HO-1 were detected by qRT-PCR and Western blot. Furthermore, inflammatory cytokines (p-NFκB, TLR4, TNF-α, IL-1β, and IL-6) and apoptosis factors (Bcl-2, Bax, and cl-casp-3) were detected by Western blot. TUNEL assay was applied to investigate apoptosis rate. Moreover, the mechanism of how MeJA played anti-oxidative stress and anti-inflammatory roles was investigated by silencing of Nrf2 via siRNA.Results: The result of MTT assay showed that MeJA improved the decreased viability of BV-2 cells induced by Aβ. The detection of MDA, SOD activity, and ROS showed the oxidative stress levels were decreased in Aβ+MeJA group compared with Aβ group. Nrf2, HO-1, and SOD were significantly up-regulated in Aβ+MeJA group compared with Aβ group (p< 0.01). In contrast, inflammatory cytokines were significantly down-regulated in Aβ+MeJA group compared with Aβ group (p< 0.05). Similarly, the expressions of apoptosis cytokines and TUNEL assay suggested a decreased apoptosis rate in Aβ+MeJA group compared to Aβ group (p< 0.01). Finally, results of Nrf2 knockdown experiment showed down-regulations of anti-oxidative stress factors (Nrf2, HO-1 and SOD), up-regulations of inflammatory cytokines, and increased ratio of Bax to Bcl in Aβ+MeJA+si-Nrf2 group compared with Aβ+MeJA group (p< 0.01).Conclusion: MeJA could relieve Aβ-induced oxidative stress and inflammatory response in microglial cells by activating Nrf2/HO-1 pathway.Keywords: methyl jasmonate, Nrf2-dependent HO-1 pathway, β-amyloid, oxidative stress, inflammatory cytokines |
| format |
article |
| author |
Li H Lv L Wu C Qi J Shi B |
| author_facet |
Li H Lv L Wu C Qi J Shi B |
| author_sort |
Li H |
| title |
Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway |
| title_short |
Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway |
| title_full |
Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway |
| title_fullStr |
Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway |
| title_full_unstemmed |
Methyl Jasmonate Protects Microglial Cells Against β-Amyloid-Induced Oxidative Stress and Inflammation via Nrf2-Dependent HO-1 Pathway |
| title_sort |
methyl jasmonate protects microglial cells against β-amyloid-induced oxidative stress and inflammation via nrf2-dependent ho-1 pathway |
| publisher |
Dove Medical Press |
| publishDate |
2020 |
| url |
https://doaj.org/article/74bfff96ebf04aaab512690a9f168496 |
| work_keys_str_mv |
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| _version_ |
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