ABSTRACT
Objective: To explore the therapeutic effect and mechanism of myricetin on disseminated intravascular coagulation (DIC). Methods: The DIC model was established by injection of 60 mg/kg LPS in KM mice, and the treatment groups were injected myricetin with different concentrations (25 or 50 mg/kg) 30 min before the model was established. Both coagulation indicators and organ function were tested, including PT, APTT, fibrinogen, AST, ALT, BUN and tissue section. In vitro, the inflammatory model of RAW 264.7 macrophage cells were established by 10 μg/mL LPS. The treatment group was treated with 50 μmol/mL myricetin for 30 min before LPS, and the expression of TNF-α and p-NF-κB was detected, further to explore the therapeutic mechanism. Results: LPS-induced DIC led to a reduction of fibrinogen and a rise of PT, APTT, AST, ALT, BUN levels, but the treatment of myricetin significantly inhibited these abnormalities. Histopathology analysis also revealed that myricetin remarkably protected the liver and renal damage. In vitro, the expression of TNF-α and p-NF-κB induced by LPS was repressed by myricetin. Conclusions: This study provides new insights into the protective effects of myricetin in LPS-induced DIC by anticoagulant and anti-inflammatory via suppressing the activation of p-NF-κB which decreased TNF-α level.
ABSTRACT
Objective: To investigate the role of ClC-3 chloride channel in the proliferation of breast cancer cell line Mcf-7 treated with curcumin and its specific mechanism. Methods: MTT assay was used to detect the effect of chloride channel blocker (DIDS) and curcumin on Mcf-7 and human normal cell viability. Patch-clamp technique was used to determine the current density before and after drug treatment. Apoptosis assay by flow cytometry was performed for further examination of cell apoptosis. Results: Curcumin had toxicity on Mcf-7 and HUVEC cells and DIDS reduced the survival rate of Mcf-7 cells by inhibiting proliferation. Curcumin could activate the chloride ion current on MCF-7 cell membrane, which would be inhibited by DIDS. Finally, curcumin in low concentration combined with DIDS could significantly promote the MCF-7 cells apoptosis. Conclusions: Our results suggest that ClC-3 protein is involved in the regulation of curcumin induced proliferation inhibiting in breast cancer cells through inducing cell apoptosis. ClC-3 may be a potential target of tumor therapy.
ABSTRACT
Objective:To explore the therapeutic effect and mechanism of myricetin on disseminated intravascular coagulation (DIC).Methods:The DIC model was established by injection of 60 mg/kg LPS in KM mice, and the treatment groups were injected myricetin with different concentrations (25 or 50 mg/kg) 30 min before the model was established. Both coagulation indicators and organ function were tested, including PT, APTT, fibrinogen, AST, ALT, BUN and tissue section. In vitro, the inflammatory model of RAW 264.7 macrophage cells were established by 10 μg/mL LPS. The treatment group was treated with 50 μmol/mL myricetin for 30 min before LPS, and the expression of TNF-α and p-NF-κB was detected, further to explore the therapeutic mechanism.Results:LPS-induced DIC led to a reduction of fibrinogen and a rise of PT, APTT, AST, ALT, BUN levels, but the treatment of myricetin significantly inhibited these abnormalities. Histopathology analysis also revealed that myricetin remarkably protected the liver and renal damage. In vitro, the expression of TNF-α and p-NF-κB induced by LPS was repressed by myricetin.Conclusions:This study provides new insights into the protective effects of myricetin in LPS-induced DIC by anticoagulant and anti-inflammatory via suppressing the activation of p-NF-κB which decreased TNF-α level.
ABSTRACT
Objective:To investigate the role of ClC-3 chloride channel in the proliferation of breast cancer cell line Mcf-7 treated with curcumin and its specific mechanism.Methods:MTT assay was used to detect the effect of chloride channel blocker (DIDS) and curcumin on Mcf-7 and human normal cell viability. Patch-clamp technique was used to determine the current density before and after drug treatment. Apoptosis assay by flow cytometry was performed for further examination of cell apoptosis.Results:Curcumin had toxicity on Mcf-7 and HUVEC cells and DIDS reduced the survival rate of Mcf-7 cells by inhibiting proliferation. Curcumin could activate the chloride ion current on MCF-7 cell membrane, which would be inhibited by DIDS. Finally, curcumin in low concentration combined with DIDS could significantly promote the MCF-7 cells apoptosis.Conclusions:Our results suggest that ClC-3 protein is involved in the regulation of curcumin induced proliferation inhibiting in breast cancer cells through inducing cell apoptosis. ClC-3 may be a potential target of tumor therapy.
ABSTRACT
Transformation of a poorly differentiated squamous cell carcinoma [SCC] of the esophagus into a [carcinosarcoma] of the pleura and lung has never been reported and its histogenetic origin is still debated. A 48-year-old man was admitted due to progressive dysphagia and a weight loss of 5 kilograms within 2 months. Upper gastrointestinal panendoscopic biopsy revealed poorly differentiated SCC of thoracic esophagus, upper third, T4N1M1 a, stage IVa. He received concurrent chemoradiotherapy [CCRT]. About 9 months later, rapid progression of lung metastases and pleural effusion were found. According to the histopathological and immunohistochemical stain results, carcinosarcoma was diagnosed. Palliative therapy was given and the patient eventually died of the disease 9 months after SCC of the thoracic esophagus was diagnosed and one month after carcinosarcoma of the pleura and lung were confirmed