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1.
J Healthc Eng ; 2022: 8387458, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35186240

RESUMEN

Cervical carcinoma is the most common gynecologic tumor in the clinic. The incidence of cervical carcinoma has been increasing in recent years, and the age of the affected population is showing a younger trend. Long-chain noncoding RNA (LncRNA) acts in the cell cycle. In cervical carcinoma, many studies have also confirmed the important role of LncRNA. LncRNA ABHD11-AS1 is one of the genes abnormally expressed in cervical carcinoma, but the specific situation has not been fully explained. This study intended to confirm whether LncRNA ABHD11-AS1 can be applied for the treatment of cervical carcinoma in the future. From January 2015 to January 2017, 72 cases of cervical carcinoma patients and 78 cases of healthy people during the same period in our hospital were selected for prospective analysis. ABHD11-AS1 and miR-1254 in serum and carcinoma tissues of cervical carcinoma patients were detected. In addition, human cervical carcinoma cells HeLa and CaSki were obtained to analyze the effects of interference with ABHD11-AS1 and miR-1254 on the biological behavior of cervical carcinoma cells. Finally, the correlation of ABHD11-AS1 with miR-1254 was verified by double fluorescein reporter enzyme and immunocoprecipitation. ABHD11-AS1 was upregulated, and miR-1254 was reduced in serum and carcinoma tissues of cervical carcinoma patients (P < 0.05). The expression levels of the two were negatively correlated (P < 0.001). ABHD11-AS1 decreased and miR-1254 increased in serum of cervical carcinoma patients after treatment (P < 0.05). High ABHD11-AS1 and low miR-1254 had a close correlation with the poor prognosis of cervical carcinoma patients (P < 0.05). Silencing LncRNA ABHD11-AS1 could inhibit the activity of cervical carcinoma cells (P < 0.05), while inhibiting miR-1254 could promote the activity of cervical carcinoma cells (P < 0.05). ENCORI online website found that LncRNA ABHD11-AS1 and miR-1254 had binding sites. Bifluorescein reporter enzyme experiment found that ABHD11-AS1-WT fluorescence activity was inhibited by transfected miR-1254-mimics (P < 0.05). LncRNA ABHD11-AS1 accelerates proliferation, invasion, and migration of cervical carcinoma cells through targeted regulation of miR-1254, which may become the key to the treatment of cervical carcinoma.


Asunto(s)
Carcinoma , MicroARNs , ARN Largo no Codificante , Neoplasias del Cuello Uterino , Carcinoma/genética , Línea Celular Tumoral , Proliferación Celular , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , MicroARNs/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Serina Proteasas/genética , Serina Proteasas/metabolismo , Neoplasias del Cuello Uterino/diagnóstico , Neoplasias del Cuello Uterino/genética , Neoplasias del Cuello Uterino/terapia
2.
Int Immunopharmacol ; 62: 309-312, 2018 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-30048861

RESUMEN

Alpinetin has been reported to have anti-inflammatory effects. However, whether alpinetin has anti-inflammatory effects in LPS-induced endometritis has not been thoroughly elucidated to date. The aim of this study was to investigate the protective effects of alpinetin on LPS-induced endometritis in mice. A mouse model of endometritis was induced by LPS and alpinetin was given 1 h before LPS treatment. According to the results, alpinetin protected mice against LPS-induced endometritis by attenuating uterine histological changes and myeloperoxidase (MPO) activity. The LPS-induced inflammatory response was inhibited by alpinetin as confirmed by the inhibition of TNF-α, IL-1ß, and IL-6 production. Furthermore, LPS-induced TLR4 expression and NF-κB activation were significantly suppressed by alpinetin. In addition, the expression of PPAR-γ was dose-dependently increased by the treatment of alpinetin. Taken together, the results of this study showed that alpinetin had protective effects against LPS-induced endometritis in mice, and the beneficial effects were occurred through the activation of PPAR-γ and inhibition of the TLR4 signaling pathway.


Asunto(s)
Antiinflamatorios/uso terapéutico , Endometritis/prevención & control , Flavanonas/uso terapéutico , Animales , Modelos Animales de Enfermedad , Relación Dosis-Respuesta a Droga , Endometritis/inmunología , Endometritis/patología , Femenino , Interleucina-1beta/antagonistas & inhibidores , Interleucina-6/antagonistas & inhibidores , Lipopolisacáridos , Ratones Endogámicos C57BL , PPAR gamma/genética , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Útero/efectos de los fármacos , Útero/inmunología , Útero/patología
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