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1.
Future Oncol ; 14(20): 2005-2011, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29513033

RESUMO

AIM: To explore the association between the determinant factors including HLA-DQB1*03, DRB1-*07, -*13 and high-risk HPV infection, the cervical squamous cell carcinoma (CSCC) pathogenesis among Chinese Uighur and Han population. MATERIALS & METHODS: HLA alleles were genotyped by PCR sequence-specific primers. RESULTS: HPV16 infection rate was significantly higher among the Uighurs and Hans with CSCC as compared with healthy controls, respectively. HLA-DQB1*03 significantly increased among Uighurs with CSCC, while HLA-DRB1*07 significantly increased among Hans with CSCC. Similar tendencies were observed for DQB1*03 with HPV16-positive Uighurs CSCC and DRB1*07 with HPV16-positive Hans CSCC. CONCLUSION: This study suggests that HLA-DQB1*03 and DRB1*07 alleles may influence the immune response to HPV16 infection and increase the risk of CSCC among the Uighurs and Hans in China.


Assuntos
Alelos , Etnicidade/genética , Predisposição Genética para Doença , Cadeias beta de HLA-DQ/genética , Neoplasias do Colo do Útero/genética , Adulto , Idoso , China/epidemiologia , Feminino , Papillomavirus Humano 16 , Humanos , Pessoa de Meia-Idade , Razão de Chances , Infecções por Papillomavirus/virologia , Medição de Risco , Análise de Sequência de DNA , Neoplasias do Colo do Útero/virologia , Adulto Jovem
2.
Afr J Tradit Complement Altern Med ; 13(4): 176-183, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-28852734

RESUMO

BACKGROUND: The current study was designed to evaluate the effect of Platycodin D (PD), triterpenoid saponins extracted from the roots of Platycodon grandiflorum (PG) on alcohol-induced fatty liver (AFL) and investigate the possible mechanism. METHODS AND MATERIALS: A rat model was set up by feeding ethanol and fish oil to experimental rats, which then were treated with PD of 10, 20, 30 mg/kg body weight/day for 4 weeks, respectively, whereafter, liver function enzymes, endotoxin of serum and liver lipid were assayed by biochemical methods, cytokines, histochemistry of hepatic tissue, the protein expression of CD14 and TLR4, the mRNA expression of MD-2, MyD 88 and TRAF-6 were assayed. RESULTS: Treatment with PD on AFL rats significantly decreased the levels of serum ALT, AST and TBIL, coefficient of liver index and the hepatic tissue contents of TG, additionally and dramatically decreased serum endotoxin levels, down-regulated MD-2 and CD14 levels, as well as the mRNA expression of TLR4, MyD88 and TRAF-6, accordingly suppressed NF-κB: p65 as well as endotoxin-mediated inflammatory factors such as TNF-α and IL-6. CONCLUSIONS: Treatment with PD effectively protects against AFL through anti-inflammatory and anti-endotoxic process, and the confirmed mechanism is that PD treatment ameliorate alcoholic-induced liver injury mainly via TLR4-MyD88-NF-K: B signal path in AFL rat. List of Abbreviations: AFL: alcoholic-induced fatty liver, CD14: cluster of differentiation 14, LPS: lipopolysaccharide, LBP: lipopolysaccharide-binding protein, TLR4: toll-like receptor 4, MD-2: molecule myeloid differential protein-2, MyD 88: myeloid differentiation primary response protein 88, TRAF-6: TNF-receptor associated factor-6, NF-κB: nuclear transcription factor kappa B, IL-6: interleukin-6, TNF-α: tumor necrosis factor-α, PG: Platycodon grandiflorum, PD: Platycodin D.


Assuntos
Álcoois/efeitos adversos , Anti-Inflamatórios/administração & dosagem , Medicamentos de Ervas Chinesas/administração & dosagem , Fígado Gorduroso/tratamento farmacológico , NF-kappa B/metabolismo , Platycodon/química , Saponinas/administração & dosagem , Receptor 4 Toll-Like/metabolismo , Triterpenos/administração & dosagem , Animais , Fígado Gorduroso/induzido quimicamente , Fígado Gorduroso/genética , Fígado Gorduroso/metabolismo , Humanos , Interleucina-6/genética , Interleucina-6/metabolismo , Masculino , NF-kappa B/genética , Raízes de Plantas/química , Ratos , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/genética , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo
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