Clinical and experimental rheumatology · 2023
Post-traumatic stress disorder and post-traumatic stress symptoms in patients with systemic autoimmune diseases during the COVID-19 pandemic.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Carmassi Claudia, Tani Chiara, Lorenzoni Valentina, Palla Ilaria, Fulvio Giovanni, Fantasia Sara, Andreozzi Gianni, Trentin Francesca, Conti Lorenzo, Gaglioti Andrea, Turchetti Giuseppe, Dell'Osso Liliana, Mosca Marta
Аннотация
OBJECTIVE: The aim of this study was to explore the effect of long non-coding ribonucleic acid (lncRNA) AK125437 on rats with postmenopausal osteoporosis via the mitogen-activated protein kinase (MAPK) pathway.
MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into three groups, including normal group, model group, and an inhibitor group, with 12 rats in each group. Only ovaries were exposed in normal group. The postmenopausal osteoporosis model was established in model group. Meanwhile, the intervention was performed with inhibitor for 3 months after modeling in inhibitor group, followed by sampling. The expression of receptor activator of nuclear factor kappa-B ligand (RANKL) was detected via immunohistochemistry. The protein expression level of phosphorylated p38 (p-p38) MAPK was determined via Western blotting (WB). Furthermore, the expression level of lncRNA AK125437 and the content of serum estradiol were determined via quantitative Polymerase Chain Reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. In addition, bone mineral density was measured using dual-energy X-ray bone mineral absorptiometer.
RESULTS: Immunohistochemistry results indicated that model group and inhibitor group had notably up-regulated positive expression level of RANKL than normal group (p<0.05), which was remarkably lower in inhibitor group than model group (p<0.05). Western blot results showed that compared with normal group, the protein expression level of p-p38 MAPK was substantially elevated in model and inhibitor groups (p<0.05). Meanwhile, the protein expression level of p-p38 MAPK was markedly lower in inhibitor group than that in model group (p<0.05). According to qPCR results, the expression level of lncRNA AK125437 was significantly up-regulated in both model group and inhibitor group compared with normal group, showing statistically significant differences (p<0.05). However, no significant differences were observed between model group and inhibitor group (p>0.05). ELISA results revealed that model group and inhibitor group had markedly lower estradiol content than normal group (p<0.05). There was no statistically significant difference in the content of estradiol between the two groups (p>0.05). According to the measurement results of bone mineral density, compared with normal group, bone mineral density was notably lower in model group and inhibitor group (p<0.05). Furthermore, it was markedly higher in inhibitor group than that of model group (p<0.05).
CONCLUSIONS: LncRNA AK125437 affects the bone mineral density of rats with postmenopausal osteoporosis by activating the MAPK pathway.
MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into three groups, including normal group, model group, and an inhibitor group, with 12 rats in each group. Only ovaries were exposed in normal group. The postmenopausal osteoporosis model was established in model group. Meanwhile, the intervention was performed with inhibitor for 3 months after modeling in inhibitor group, followed by sampling. The expression of receptor activator of nuclear factor kappa-B ligand (RANKL) was detected via immunohistochemistry. The protein expression level of phosphorylated p38 (p-p38) MAPK was determined via Western blotting (WB). Furthermore, the expression level of lncRNA AK125437 and the content of serum estradiol were determined via quantitative Polymerase Chain Reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. In addition, bone mineral density was measured using dual-energy X-ray bone mineral absorptiometer.
RESULTS: Immunohistochemistry results indicated that model group and inhibitor group had notably up-regulated positive expression level of RANKL than normal group (p<0.05), which was remarkably lower in inhibitor group than model group (p<0.05). Western blot results showed that compared with normal group, the protein expression level of p-p38 MAPK was substantially elevated in model and inhibitor groups (p<0.05). Meanwhile, the protein expression level of p-p38 MAPK was markedly lower in inhibitor group than that in model group (p<0.05). According to qPCR results, the expression level of lncRNA AK125437 was significantly up-regulated in both model group and inhibitor group compared with normal group, showing statistically significant differences (p<0.05). However, no significant differences were observed between model group and inhibitor group (p>0.05). ELISA results revealed that model group and inhibitor group had markedly lower estradiol content than normal group (p<0.05). There was no statistically significant difference in the content of estradiol between the two groups (p>0.05). According to the measurement results of bone mineral density, compared with normal group, bone mineral density was notably lower in model group and inhibitor group (p<0.05). Furthermore, it was markedly higher in inhibitor group than that of model group (p<0.05).
CONCLUSIONS: LncRNA AK125437 affects the bone mineral density of rats with postmenopausal osteoporosis by activating the MAPK pathway.