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/metabolismoRESUMO
Giant congenital melanocytic nevi are rare, with an estimated incidence of approximately 1 in 20,000 live births. They increase the lifetime risk for malignant melanoma and neurological deficits, including leptomeningeal melanocytosis and epilepsy. Recently, we encountered two patients in whom giant congenital melanocytic nevi were noted at birth. Case 1 presented with the largest nevus spreading across the posterior scalp, neck, chest wall, shoulder and upper back. At the age of 2 months, magnetic resonance imaging (MRI) was performed and no leptomeningeal melanocytosis was found. Case 2 presented with a huge nevus covering most parts of the lower abdomen, lower back, buttocks and bilateral upper thighs. She also had normal MRI findings in the newborn period. At the age of 7 years, leptomeningeal thickening on the surface of the junction between the pons and midbrain was found on brain MRI although she was neurologically asymptomatic. Here, we describe these two cases with congenital melanocytic nevi and review the literature about its clinical manifestations, outcomes, risks for malignant melanoma and neurocutaneous melanosis, and possible surgical interventions.
Assuntos
Nevo Pigmentado/congênito , Neoplasias Cutâneas/congênito , Adulto , Feminino , Humanos , Recém-Nascido , Masculino , Nevo Pigmentado/patologia , Nevo Pigmentado/cirurgia , Gravidez , Neoplasias Cutâneas/patologia , Neoplasias Cutâneas/cirurgiaRESUMO
AIM: To study the effects of some bioflavonoids on the gossypol-induced hypokalemia. METHODS: The 11beta-hydroxysteroid dehydrogenase (11beta-OHSD) protein was prepared from guinea pig kidney. The activity of 11beta-OHSD with NAD as the coenzyme was measured by HPLC. The drug interaction was analysed by isobolographic method. RESULTS: The 11beta-OHSD can be inhibited by some bioflavonoids. The IC50 (95 % confidence limits) values were: quercetin 164 (79 - 341) micromol/L, morin 913 (385 - 2173) micromol/L, and naringenin 2193 (1114 - 4315) micromol/L. When the 11beta-OHSD was treated with quercetin, tangeretin, morin, naringenin plus gossypol, the combination index (CI) values were 0.92, 0.85, 0.98, and 1.01 respectively. CONCLUSION: The interaction of some bioflavonoids with gossypol might be one of the factors for gossypol-induced hypokalemia.
