Ghaida Alsaif, N. Almosnid, Chun-Xia He, E. Altman, Ying Gao
Background: The oligostilbenes cis - and trans -gnetin H were previously studied for their ability to inhibit cancer cell proliferation and induce apoptosis. However, an in-depth understanding of the proteins involved in this process remains poorly understood. Methods: The ability of cis - and trans -gnetin H to act as an antioxidant by scavenging one of the stable free radicals DPPH was tested. We also tested the ability of both compounds to generate oxidative stress through elevating the reactive oxygen species (ROS) resulting in apoptosis using lung cancer cell line A549. Also, immunoassay Enzyme-linked Immunosorbent Assay (ELISA) was performed to test the levels of the major apoptotic proteins using a negative estrogen receptor (ER-) breast cancer cell line MDA-MB-231. Results: Cis - and trans -gnetin H treatment showed a high percentage of the radical scavenging activity =%24 at the lowest concentration 12.5μM (p≤0.0001) and elevated the levels of ROS in A549 to 50%, 45%, respectively (p≤0.001). In addition, cis - and trans -gnetin H induced early apoptosis in A549 cell line to 59% and 38.9%, respectively, at the highest concentration of 25μM compared to the untreated control (p≤0.0001). Results from apoptosis protein array showed certain up-regulated proteins such as Bid, Bad, cytochrome c, FasL, TRAIL1-4 and down regulated proteins such as XIAP, surviving, Hsp60, suggesting inducing apoptosis was facilitated by cross talk between intrinsic and extrinsic pathway through TRAIL pathway. Conclusion: These observations suggested that cis - and trans -gnetin H induces apoptosis in human lung and breast cancer cells in vitro through elevating the levels of oxidative stress and directly affecting the primary regulator of apoptosis proteins.
{"title":"The Resveratrol Oligomers Cis- and Trans-gnetin H Inhibit Human Cancer Cells by Induction of Apoptosis and Oxidative Stress","authors":"Ghaida Alsaif, N. Almosnid, Chun-Xia He, E. Altman, Ying Gao","doi":"10.30654/mjps.10007","DOIUrl":"https://doi.org/10.30654/mjps.10007","url":null,"abstract":"Background: The oligostilbenes cis - and trans -gnetin H were previously studied for their ability to inhibit cancer cell proliferation and induce apoptosis. However, an in-depth understanding of the proteins involved in this process remains poorly understood. Methods: The ability of cis - and trans -gnetin H to act as an antioxidant by scavenging one of the stable free radicals DPPH was tested. We also tested the ability of both compounds to generate oxidative stress through elevating the reactive oxygen species (ROS) resulting in apoptosis using lung cancer cell line A549. Also, immunoassay Enzyme-linked Immunosorbent Assay (ELISA) was performed to test the levels of the major apoptotic proteins using a negative estrogen receptor (ER-) breast cancer cell line MDA-MB-231. Results: Cis - and trans -gnetin H treatment showed a high percentage of the radical scavenging activity =%24 at the lowest concentration 12.5μM (p≤0.0001) and elevated the levels of ROS in A549 to 50%, 45%, respectively (p≤0.001). In addition, cis - and trans -gnetin H induced early apoptosis in A549 cell line to 59% and 38.9%, respectively, at the highest concentration of 25μM compared to the untreated control (p≤0.0001). Results from apoptosis protein array showed certain up-regulated proteins such as Bid, Bad, cytochrome c, FasL, TRAIL1-4 and down regulated proteins such as XIAP, surviving, Hsp60, suggesting inducing apoptosis was facilitated by cross talk between intrinsic and extrinsic pathway through TRAIL pathway. Conclusion: These observations suggested that cis - and trans -gnetin H induces apoptosis in human lung and breast cancer cells in vitro through elevating the levels of oxidative stress and directly affecting the primary regulator of apoptosis proteins.","PeriodicalId":251442,"journal":{"name":"Mathews Journal of Pharmaceutical Science","volume":"61 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126247989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Osteoclasts are multinucleated bone degrading cells that differentiate from monocyte/macrocphage precursors of the hematopoietic system. From the bone marrow, precursors of osteoclasts move towards the systemic circulation through the attraction towards chemokines in the blood and are later taken up by various resorption sites where they undergo differentiation into osteoclasts. Macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-ҡB ligand (RANKL) play a pivotal role in the differentiation and activation of osteoclasts. M-CSF induces the expression of RANK on myeloid progenitors and RANKL activates its receptor to initiate osteoclast differentiation. RANKL also stimulates bone resorption in mature osteoclasts. Rheumatoid arthritis is an autoimmune disease that leads to severe bone destruction mediated by the abnormal activation of osteoclasts. Synovial tissues in rheumatoid arthritis produce inflammatory cytokines that act on osteoclast precursor cells, thereby differentiating them into osteoclasts by cooperating with RANKL. Bone resorption proceeds uncontrollably through the abnormal activity of osteoclasts, leading to bone and cartilage destruction in the joints. The involvement of osteoclasts in the pathogenesis of rheumatoid arthritis has been further confirmed through animal model studies.
{"title":"Role of Osteoclast Regulation in Arthritis – A Review","authors":"A. Iqbal","doi":"10.30654/mjps.10006","DOIUrl":"https://doi.org/10.30654/mjps.10006","url":null,"abstract":"Osteoclasts are multinucleated bone degrading cells that differentiate from monocyte/macrocphage precursors of the hematopoietic system. From the bone marrow, precursors of osteoclasts move towards the systemic circulation through the attraction towards chemokines in the blood and are later taken up by various resorption sites where they undergo differentiation into osteoclasts. Macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-ҡB ligand (RANKL) play a pivotal role in the differentiation and activation of osteoclasts. M-CSF induces the expression of RANK on myeloid progenitors and RANKL activates its receptor to initiate osteoclast differentiation. RANKL also stimulates bone resorption in mature osteoclasts. Rheumatoid arthritis is an autoimmune disease that leads to severe bone destruction mediated by the abnormal activation of osteoclasts. Synovial tissues in rheumatoid arthritis produce inflammatory cytokines that act on osteoclast precursor cells, thereby differentiating them into osteoclasts by cooperating with RANKL. Bone resorption proceeds uncontrollably through the abnormal activity of osteoclasts, leading to bone and cartilage destruction in the joints. The involvement of osteoclasts in the pathogenesis of rheumatoid arthritis has been further confirmed through animal model studies.","PeriodicalId":251442,"journal":{"name":"Mathews Journal of Pharmaceutical Science","volume":"66 4","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121014444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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