Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway
BackgroundIt has been found that fluoride may cause cardiomyocyte damage. c-Jun N-terminal kinases (JNK) signaling pathway plays an important role in apoptosis, but its role in fluorosis-induced cardiomyocyte damage is still unknown yet. ObjectiveTo explore the toxic effect of sodium fluoride (NaF)...
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| Format: | Article |
| Language: | English |
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Editorial Committee of Journal of Environmental and Occupational Medicine
2023-02-01
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| Series: | 环境与职业医学 |
| Subjects: | |
| Online Access: | http://www.jeom.org/article/cn/10.11836/JEOM22322 |
| _version_ | 1811154234840711168 |
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| author | Liting CAO Wei XU Baohui MA |
| author_facet | Liting CAO Wei XU Baohui MA |
| author_sort | Liting CAO |
| collection | DOAJ |
| description | BackgroundIt has been found that fluoride may cause cardiomyocyte damage. c-Jun N-terminal kinases (JNK) signaling pathway plays an important role in apoptosis, but its role in fluorosis-induced cardiomyocyte damage is still unknown yet. ObjectiveTo explore the toxic effect of sodium fluoride (NaF) on H9c2 cardiomyocytes of rats and whether NaF affects cardiomyocyte apoptosis through the JNK signaling pathway. MethodsAccording to the concentrations of sodium fluoride and whether sp600125 (JNK inhibitor) was added, cardiomyocytes of rats were divided into six groups, including control group, SP600125 group (SP group), 0.24, 0.48, and 0.96 mmol·L−1 NaF groups, and 0.96 mmol·L−1 NaF+SP600125 group (NaF+SP group). Cardiomyocytes exposed to NaF for 24 h were observed using a fluorescence inverted microscope. The changes of cell viability at 24, 48, and 72 h after the treatment were detected by CCK-8 method. The levels of reactive oxygen species (ROS) at 24 h after the treatment in H9c2 cardiomyocytes were determined by fluorescent probe method. The expression levels of Bcl-2, Bax, Caspase-3, and JNK mRNA at 24 h after the treatment were detected by real-time PCR. The protein expression levels of Bcl-2, Bax, Caspase-3, and p-JNK at 24 h after the treatment were detected by Western blotting. ResultsCompared with the control group, after being exposed to 0.48 and 0.96 mmol·L−1 NaF for 24 h, the cell growth density decreased. With the increase of NaF concentration, rounded cells and some suspended dead cells appeared. At 24h after exposure to NaF, the cell viability of the 0.48 and 0.96 mmol·L−1 NaF groups decreased compared with the control group (P<0.05). At 48h and 72h after exposure to NaF, the cell viability levels of the NaF treated groups were significantly lower than that of the control group (P<0.05). After NaF exposure for 24 h, compared with the control group, the intracellular ROS levels were increased (P<0.05); the mRNA expression levels of Bcl-2 were decreased to varying degrees, especially in the 0.48 and 0.96 mmol·L−1 NaF groups (P<0.05); the mRNA expression levels of Bax, Caspase-3, and JNK were increased (P<0.05); the protein expression levels of Bcl-2 were reduced (P<0.05); the protein expression levels of Bax, Caspase-3, and p-JNK were elevated (P<0.05). Compared with the 0.96 mmol·L−1 NaF group, the cell viability of the NaF+SP group was increased, the intracellular ROS level was decreased, the mRNA expression levels of Bax, Caspase-3, and JNK were decreased, the protein expression level of Bcl-2 was increased, and the protein expression levels of Bax, Caspase-3, and p-JNK were decreased (P<0.05); the expression level of Bcl-2 mRNA had a rising trend but showed no statistical significance (P>0.05). ConclusionCardiomyocyte damage after excessive fluoride exposure may result from fluoride inducing excessive ROS production in cardiomyocytes, which may activate the JNK signaling pathway and induce cardiomyocyte apoptosis. |
| first_indexed | 2024-04-10T04:12:15Z |
| format | Article |
| id | doaj.art-f911c6b07ff54cbbb01498aeb3538e75 |
| institution | Directory Open Access Journal |
| issn | 2095-9982 |
| language | English |
| last_indexed | 2024-04-10T04:12:15Z |
| publishDate | 2023-02-01 |
| publisher | Editorial Committee of Journal of Environmental and Occupational Medicine |
| record_format | Article |
| series | 环境与职业医学 |
| spelling | doaj.art-f911c6b07ff54cbbb01498aeb3538e752023-03-13T02:17:08ZengEditorial Committee of Journal of Environmental and Occupational Medicine环境与职业医学2095-99822023-02-0140222422910.11836/JEOM2232222322Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathwayLiting CAO0Wei XU1Baohui MA2Department of Physiology/Institute of Neuroscience, Baotou Medical College, Baotou, Inner Mongolia 014040, ChinaDepartment of Physiology/Institute of Neuroscience, Baotou Medical College, Baotou, Inner Mongolia 014040, ChinaDepartment of Physiology/Institute of Neuroscience, Baotou Medical College, Baotou, Inner Mongolia 014040, ChinaBackgroundIt has been found that fluoride may cause cardiomyocyte damage. c-Jun N-terminal kinases (JNK) signaling pathway plays an important role in apoptosis, but its role in fluorosis-induced cardiomyocyte damage is still unknown yet. ObjectiveTo explore the toxic effect of sodium fluoride (NaF) on H9c2 cardiomyocytes of rats and whether NaF affects cardiomyocyte apoptosis through the JNK signaling pathway. MethodsAccording to the concentrations of sodium fluoride and whether sp600125 (JNK inhibitor) was added, cardiomyocytes of rats were divided into six groups, including control group, SP600125 group (SP group), 0.24, 0.48, and 0.96 mmol·L−1 NaF groups, and 0.96 mmol·L−1 NaF+SP600125 group (NaF+SP group). Cardiomyocytes exposed to NaF for 24 h were observed using a fluorescence inverted microscope. The changes of cell viability at 24, 48, and 72 h after the treatment were detected by CCK-8 method. The levels of reactive oxygen species (ROS) at 24 h after the treatment in H9c2 cardiomyocytes were determined by fluorescent probe method. The expression levels of Bcl-2, Bax, Caspase-3, and JNK mRNA at 24 h after the treatment were detected by real-time PCR. The protein expression levels of Bcl-2, Bax, Caspase-3, and p-JNK at 24 h after the treatment were detected by Western blotting. ResultsCompared with the control group, after being exposed to 0.48 and 0.96 mmol·L−1 NaF for 24 h, the cell growth density decreased. With the increase of NaF concentration, rounded cells and some suspended dead cells appeared. At 24h after exposure to NaF, the cell viability of the 0.48 and 0.96 mmol·L−1 NaF groups decreased compared with the control group (P<0.05). At 48h and 72h after exposure to NaF, the cell viability levels of the NaF treated groups were significantly lower than that of the control group (P<0.05). After NaF exposure for 24 h, compared with the control group, the intracellular ROS levels were increased (P<0.05); the mRNA expression levels of Bcl-2 were decreased to varying degrees, especially in the 0.48 and 0.96 mmol·L−1 NaF groups (P<0.05); the mRNA expression levels of Bax, Caspase-3, and JNK were increased (P<0.05); the protein expression levels of Bcl-2 were reduced (P<0.05); the protein expression levels of Bax, Caspase-3, and p-JNK were elevated (P<0.05). Compared with the 0.96 mmol·L−1 NaF group, the cell viability of the NaF+SP group was increased, the intracellular ROS level was decreased, the mRNA expression levels of Bax, Caspase-3, and JNK were decreased, the protein expression level of Bcl-2 was increased, and the protein expression levels of Bax, Caspase-3, and p-JNK were decreased (P<0.05); the expression level of Bcl-2 mRNA had a rising trend but showed no statistical significance (P>0.05). ConclusionCardiomyocyte damage after excessive fluoride exposure may result from fluoride inducing excessive ROS production in cardiomyocytes, which may activate the JNK signaling pathway and induce cardiomyocyte apoptosis.http://www.jeom.org/article/cn/10.11836/JEOM22322sodium fluorideh9c2 cardiomyocytejnk signaling pathwayapoptosisoxidative stressreactive oxygen species |
| spellingShingle | Liting CAO Wei XU Baohui MA Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway 环境与职业医学 sodium fluoride h9c2 cardiomyocyte jnk signaling pathway apoptosis oxidative stress reactive oxygen species |
| title | Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway |
| title_full | Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway |
| title_fullStr | Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway |
| title_full_unstemmed | Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway |
| title_short | Effect of sodium fluoride on myocardial damage by regulating apoptosis through JNK signaling pathway |
| title_sort | effect of sodium fluoride on myocardial damage by regulating apoptosis through jnk signaling pathway |
| topic | sodium fluoride h9c2 cardiomyocyte jnk signaling pathway apoptosis oxidative stress reactive oxygen species |
| url | http://www.jeom.org/article/cn/10.11836/JEOM22322 |
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