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1.
Subst Use Misuse ; 59(7): 1110-1114, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38403986

RESUMO

Background: The prevalence of cannabis use in the United Kingdom might be underestimated using the Crime Survey of England and Wales. The current study examined whether responding to questions about their cannabis use as part of a crime survey would be less likely to report that they use cannabis compared to those responding to the same questions that are part of a survey about health. Methods: Participants were randomized to be told that the items about cannabis use came from a crime survey versus from a health survey. In addition, the sample was recruited using a representative online sampling method and compared to published rates of self-reported cannabis use collected as part of the Crime Survey for England and Wales. Results: There was no significant difference (p > 0.05) in the proportion endorsing cannabis use between those told the items came from a crime survey versus a health survey. However, self-reported rates of cannabis use collected as part of the online panel (51.3% ever use; 11.9% past year; age range 18-64 years) appeared higher than those reported based on results from the Crime Survey for England and Wales (37.2% ever and 5.8% past year; age range 18-59 years). Conclusion: The current study did not find evidence that manipulating whether participants were told that the items asking about cannabis use came from a survey asking about criminal activity versus one about health had an impact on self-reported cannabis use. However, as prevalence estimates generated by the Crime Survey of England and Wales do appear to be an underestimate of actual levels of cannabis use in the United Kingdom, further research is merited on this topic.


Assuntos
Cannabis , Criminosos , Humanos , Adolescente , Adulto Jovem , Adulto , Pessoa de Meia-Idade , Prevalência , Reino Unido/epidemiologia , Inglaterra/epidemiologia , Nicotiana
2.
Tumour Biol ; 39(4): 1010428317697555, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28443459

RESUMO

Astragaloside IV, the active component of Astragalus membranaceus, exhibits diverse biological roles including the anti-tumor activity. In this study, we evaluated the chemosensitive role of astragaloside IV in non-small cell lung cancer cells. Cell Counting Kit-8 analysis was performed to determine cell viability. Real-time polymerase chain reaction and western blot were used to measure the messenger RNA and protein expression. Results showed that astragaloside IV treatment could suppress the proliferation of non-small cell lung cancer cells. In addition, combined treatment with astragaloside IV remarkably enhanced the chemosensitivity to gefitinib in three non-small cell lung cancer cell lines including NCI-H1299, HCC827, and A549. Furthermore, compared with gefitinib-treated cells, the messenger RNA expression of SIRT6 was obviously increased in non-small cell lung cancer cells treated with gefitinib combined with astragaloside IV. In addition, downregulation of SIRT6 was accomplished using small interference RNA technology. As a result, SIRT6 inhibition abolished the sensitization role of astragaloside IV in non-small cell lung cancer cells. Taken together, these data demonstrated that astragaloside IV sensitized tumor cells to gefitinib via regulation of SIRT6, suggesting that astragaloside IV may serve as potential therapeutic approach for lung cancer.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Quinazolinas/administração & dosagem , Saponinas/administração & dosagem , Sirtuínas/biossíntese , Triterpenos/administração & dosagem , Células A549 , Apoptose/efeitos dos fármacos , Astragalus propinquus/química , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma Pulmonar de Células não Pequenas/patologia , Proliferação de Células/efeitos dos fármacos , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Resistencia a Medicamentos Antineoplásicos/genética , Medicamentos de Ervas Chinesas/administração & dosagem , Medicamentos de Ervas Chinesas/química , Gefitinibe , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Sirtuínas/genética
3.
Cell Physiol Biochem ; 40(5): 1221-1229, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27960166

RESUMO

BACKGROUND: Chemoresistance is a major obstacle to successful chemotherapy for human non-small cell lung cancer (NSCLC). Astragaloside IV, the component of Astragalus membranaceus, has been reported to exhibit anti-inflammation, anti-cancer and immunoregulatory properties. In the present study, we investigated the role of astragaloside IV in the chemoresistance to cisplatin in NSCLC cells. METHODS: We established astragaloside IV-suppressed NSCLC cell lines including A549, HCC827, and NCI-H1299 and evaluated their sensitivity to cisplatin in vitro. In addition, we examined the mRNA and protein levels of B7-H3 in response to cisplatin-based chemotherapy. RESULTS: We showed that high doses of astragaloside IV (10, 20, 40 ng/ml) inhibited NSCLC cell growth, whereas low concentrations of astragaloside IV (1, 2.5, 5 ng/ml) had no obvious cytotoxicity on cell viability. Moreover, combined treatment with astragaloside IV significantly increased chemosensitivity to cisplatin in NSCLC cells. On the molecular level, astragaloside IV co-treatment significantly inhibited the mRNA and protein levels of B7-H3 in the presence of cisplatin. In addition, ectopic expression of B7-H3 diminished the sensitization role of astragaloside IV in cellular responses to cisplatin in NSCLC cells. CONCLUSION: These results demonstrate that astragaloside IV enhances chemosensitivity to cisplatin via inhibition of B7-H3 and that treatment with astragaloside IV and inhibition of B7-H3 serve as potential therapeutic approach for lung cancer patients.


Assuntos
Antígenos B7/metabolismo , Carcinoma Pulmonar de Células não Pequenas/patologia , Cisplatino/farmacologia , Neoplasias Pulmonares/patologia , Saponinas/farmacologia , Triterpenos/farmacologia , Apoptose/efeitos dos fármacos , Antígenos B7/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Neoplasias Pulmonares/genética
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