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Through the traditional Chinese medicine inheritance platform system, with the help of medical records, Ye Tianshi and Wu Jutong's medication characteristics for summer heat sickness were analyzed, the laws of the two people's medication were summarized, and the similarities and differences between the two were explored to explore the relationship. As a result, it was found that both of them recognized the relationship between summer heat and wetness, and Wu Jutong believed that "wind" was also an important pathogenic factor. Both of the patients were treated with cold medicine and warm medicine. They used mostly bitter, sweet, pungent taste and lungs, spleen, stomach, and heart meridian are the main components; two are commonly used Armeniacae Semen Amarum, Talcum, Rehmanniae Radix, Ophiopogonis Radix, Pinelliae Rhizoma and other drugs, Ye Tianshi use Scrophulariae Radix, Tetrapanacis Medulla, Coicis Semen and other drugs more, Wu Jutong use Gypsum Fibrosum, Sojae Semen Praeparatum, Menthae Haplocalycis Herba and other drugs more; at the same time, a combination of two high-frequency medicines used by two people has been excavated, and a new prescription has been deduced to provide a reference for further understanding and treatment of summer diseases.
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Objective To investigate the association of lovastatin overcoming gefitinib resistance with the levels of integrin β1 and Survivin in human non-small cell lung cancer (NSCLC) cell line PC9 in vitro, and to explore the possible mechanism. Methods The NSCLC cell line PC9 with acq uired gefitini-resistance were divided into 4 groups; control group (RPM1 1640), gefitinib group (1 /μmol/L gefitinib), lovastatin group (5 μmol/L lovastatin), and gefitinib combined with lovastatin group (1 μmol/L gefitinib+5 /μmol L lovastatin). After treatment with different drugs in each group, the inhibition of cell proliferation was detected by cell counting kit-8 (CCK-8) test, the levels of integrin ft 1 and Survivin mRNA were detected by PCR, and the expressions of integrin (31 and Survivin protein were detected by Western blotting analysis. Results Compared with the control group, lovastatin group and gefitinib group, lovastatin combined with gefitinib treatment had significantly inhibited proliferation of PC9 cells with acquired gefitinib-resistance (P<0. 01), and the expressions of integrin)31. Survivin protein and mRNA in PC9 cells were significantly decreased in the three groups (P<0. 05, P<0. 01). Conclusion Mechanisms of lovastatin combined with gefitinib in overcoming gefitinib resistance may be through blocking integrin β1-p-Akt-Survivin signaling pathway, indicating that the combination treatment might be an effective strategy for gefitinib resistance.
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Objective To investigate the value of fractional exhaled nitric oxide (FeNO) in the treatment of asthma-chronic obstructive pulmonary disease overlap syndrome (ACOS). Methods The twenty-eight ACOS patients receiving no standardmedication treatment were recruited from May 2015 to Oct. 2015 in Suzhou Kowloon Hospital; the patients inhaled corticosteroids/long-acting beta agonist (ICS/LABA) for 12 weeks and the changes of FeNO levels, FEV1%pred, induced sputum eosinophil (EOS), blood total IgE, and high sensitivity C-reactive protein (hs-CRP) were examined before and after treatment. The correlations between FeNO and other indices were analyzedby Pearson correlation coefficient method. The patients were divided into different groups according to different age and smoking statuses, and the changes of the indices before and after treatment were compared between different groups. Twenty-eight healthy participants were recruited as control group and their FeNO levels were also tested. Results After treatment, the FeNO levels ([32. 04±8. 34] × 10-9 mol/L vs [25. 56 ±13] ×10-9 mol/L, P<0. 05), induced sputum EOS ([18. 51 ± 5. 36]% vs [13. 18 ± 1. 56]%, P<0. 05), and blood total IgE ([251. 91 ± 42. 24] ng/mL vs [204. 65 ± 28. 52] ng/mL, P<0. 05) of ACOS patients were significantly lower than those before treatment. There was no significant difference in FEV1%pred ([52. 03 ± 7. 03-% vs [55. 16 ± 8. 20-%, P = 0. 391) or hs-CRP ([10. 86 ± 4. 92- mg/L vs [9. 16 ± 1. 82) mg/L, P = 0. 077) before and after treatment in ACOS patients. Meanwhile, the levels of FeNO in ACOS group were significantly higher than those in the healthy control group before and after treatment ([32. 04±8. 34-×10-9 mol/L, [25. 56 ± 4. 13×10-9 mol/L vs [17. 04+0. 97×10-9 mol/L,P<0. 05). The levels of FeNO, induced sputum EOS and serum total IgE were significantly different among different ages and smoking status before and after ICS/LABA treatment. The pre- and post-treatment FeNO levels were positively correlated with induced sputum EOS and serum total IgE (pre-treatment; r=S 92S, P<0. 01 and s=S I4I, P<0. 01; sost-treatment; r=0. 247, P<0. 01 and r=0. 443, P<0. 01); while it was not correlated with serumhs-CRP or FEV1%pred. Conclusion Our findings indicate that eosinophilic inflammation is present in the airways of ACOS patients, which can be treated with ICS/LABA inhalation. The curative effect is not affected by age or smoking status. FeNO detection can be used to evaluate the efficacy of ICS/LABA for ACOS, which is associated with induced sputum EOS and serum total IgE.
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<p><b>OBJECTIVE</b>To observe effect of Shufeng Xuanfei Recipe (SXR) and Jiebiao Qingli Recipe (JQR) on mRNA and protein expressions of Toll-like receptor 7 (TLR7), myeloid differentiation factor 88 (MyD88), and nuclear factor-kappaB (NF-kappaB) in mice infected with influenza virus FM1.</p><p><b>METHODS</b>One hundred and eight mice were randomly divided into nine groups, i.e., the normal control group, the model group, the Oseltamivir group (at the daily dose of 2.5 g/mL), the high dose SXR group (at the daily dose of 3.762 g/kg), the middle dose SXR group (at the daily dose of 1.881 g/kg), the low dose SXR group (at the daily dose of 0.941 g/kg), the high dose JQR group (at the daily dose of 4.368 g/kg), the middle dose JQR group (at the daily dose of 2.184 g/kg), and the low dose JQR group (at the daily dose of 1.092 g/kg), 12 in each group. All mice were mildly anesthetized by ether. Mice in the normal control group were treated by nasal drop of 0.05 mL normal saline, while mice in the rest groups were infected by nasal drop of 0.05 mL influenza virus strain FM1 (LD50). The successful modeling rate was 100%. All medication was performed by gastrogavage 2 h after infection. Distilled water was given by gastrogavage to mice in the normal control group and the model group at the daily dose of 0.2 mL, each time per day for 4 successive days. mRNA expressions of TLR7, MyD88, and NF-kappaB in the lung tissue were determined by Western blot.</p><p><b>RESULTS</b>Compared with the normal control group, mRNA expressions of TLR7, MyD88, and NF-kappaB increased in the model group (P < 0.01). Compared with the model group, mRNA and protein expressions of TLR7, MyD88, and NF-kappaB decreased in the Oseltamivir group, the high, middle, and low dose SXR groups (P < 0.05, P < 0.01); mRNA and protein expressions of TLR7 and NF-kappaB decreased in the high and middle dose JQR groups (P < 0.05, P < 0.01); mRNA expressions of MyD88 decreased in the high and middle dose JQR groups (P < 0.05); protein expressions of MyD88 decreased in the middle dose JQR group (P < 0.05); protein expressions of TLR7 and NF-kappaB decreased in the low dose JQR group (P < 0.05). Compared with the Oseltamivir group, protein expressions of MyD88 decreased in the low dose SXR group (P < 0.05); protein expressions of NF-kappaB decreased in the middle and low dose SXR groups (P < 0.01); mRNA and protein expressions of TLR7 (P < 0.05, P < 0.01), and protein expressions of MyD88 (P < 0.01) decreased in the high, middle, and low dose JQR groups; mRNA and protein expressions of NF-kappaB decreased in the low dose JQR group (P < 0.05, P < 0.01).</p><p><b>CONCLUSIONS</b>Each dose SXR and middle dose JQR could down-regulating the activity of NF-kappaB through adjusting MyD88 dependent TLR signal pathway, thus fighting against influenza virus. SXR was more effective than JQR.</p>
Sujets)
Animaux , Mâle , Souris , Médicaments issus de plantes chinoises , Pharmacologie , Utilisations thérapeutiques , Poumon , Métabolisme , Glycoprotéines membranaires , Génétique , Métabolisme , Souris de lignée ICR , Facteur de différenciation myéloïde-88 , Génétique , Métabolisme , Facteur de transcription NF-kappa B , Génétique , Métabolisme , Orthomyxoviridae , Infections à Orthomyxoviridae , Traitement médicamenteux , Métabolisme , Pneumopathie virale , Traitement médicamenteux , Métabolisme , ARN messager , Génétique , Transduction du signal , Récepteur de type Toll-7 , Génétique , MétabolismeRésumé
Gefitinib, a tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR), is presently used to treat the patients previously undergoing platinum-based chemotherapy for advanced non-small cell lung cancer (NSCLC). However, acquired resistance to EGFR-targeting drugs has become a significant problem. Currently, the theory of secondary mutation of EGFR gene was widely accepted in this area. Meanwhile, some studies have shown that gefitinib resistance was related to drug transport, EGFR/Met gene amplification and the changes in signaling pathway, which indicates that this theory can not completely explain the mechanism of acquired drug-resistance. This review will summarize the mechanism of gefitinib resistance, and address the new strategies to overcome this acquired drug-resistance.