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1.
Biomed Pharmacother ; 165: 115266, 2023 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-37541177

RESUMEN

Inflammatory bowel disease (IBD) encompasses a collection of idiopathic diseases characterized by chronic inflammation in the gastrointestinal (GI) tract. Patients diagnosed with IBD often experience necessitate long-term pharmacological interventions. Among the multitude of administration routes available for treating IBD, oral administration has gained significant popularity owing to its convenience and widespread utilization. In recent years, there has been extensive evaluation of the efficacy of orally administered herbal medicinal products and their extracts as a means of treating IBD. Consequently, substantial evidence has emerged, supporting their effectiveness in IBD treatment. This review aimed to provide a comprehensive summary of recent studies evaluating the effects of herbal medicinal products in the treatment of IBD. We delved into the regulatory role of these products in modulating immunity and maintaining the integrity of the intestinal epithelial barrier. Additionally, we examined their impact on antioxidant activity, anti-inflammatory properties, and the modulation of intestinal flora. By exploring these aspects, we aimed to emphasize the significant advantages associated with the use of oral herbal medicinal products in the treatment of IBD. Of particular note, this review introduced the concept of herbal plant-derived exosome-like nanoparticles (PDENs) as the active ingredient in herbal medicinal products for the treatment of IBD. The inclusion of PDENs offers distinct advantages, including enhanced tissue penetration and improved physical and chemical stability. These unique attributes not only demonstrate the potential of PDENs but also pave the way for the modernization of herbal medicinal products in IBD treatment.


Asunto(s)
Enfermedades Inflamatorias del Intestino , Plantas Medicinales , Humanos , Fitoterapia , Medicina de Hierbas , Enfermedades Inflamatorias del Intestino/tratamiento farmacológico
2.
Chem Biol Interact ; 317: 108939, 2020 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-31945315

RESUMEN

Cantharidin (CTD) is a traditional Chinese medicine that shows an anticancer effects in multiple types of cancer cells. However, the mechanism of CTD anti-cancer function in gastric cancer (GC) is still unclear. The aim of the present study was to investigate the underlying mechanism that CTD inhibits proliferation and migration through suppression of the PI3K/Akt signaling. CTD induced GC cell apoptosis and inhibited metastasis measured by CCK8 assays as well as wound healing assays and transwell assays. Mechanistic investigations suggested that CTD modulated the PI3K/Akt signaling via western-blot and quantitative q-PCR. In addition, we identified and confirmed CCAT1 as a novel direct target of CTD inhibited PI3K/AKt signaling expression. In conclusion, our results provide new point into the critical role of CTD in suppressing PI3K/Akt signaling via down-regulation of CCAT1, resulting in suppression GC cell growth and migration/invasion.


Asunto(s)
Cantaridina/farmacología , Movimiento Celular/efectos de los fármacos , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , ARN Largo no Codificante/metabolismo , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Humanos , Fosfohidrolasa PTEN/genética , Fosfohidrolasa PTEN/metabolismo , Fosfatidilinositol 3-Quinasas/genética , Proteínas Proto-Oncogénicas c-akt/genética , ARN Largo no Codificante/genética , Transducción de Señal/efectos de los fármacos , Neoplasias Gástricas
3.
Gastroenterology ; 156(8): 2230-2241.e11, 2019 06.
Artículo en Inglés | MEDLINE | ID: mdl-30742832

RESUMEN

BACKGROUND & AIMS: We performed a nationwide, retrospective study to determine the incidence and causes of drug-induced liver injury (DILI) in mainland China. METHODS: We collected data on a total of 25,927 confirmed DILI cases, hospitalized from 2012 through 2014 at 308 medical centers in mainland China. We collected demographic, medical history, treatment, laboratory, disease severity, and mortality data from all patients. Investigators at each site were asked to complete causality assessments for each case whose diagnosis at discharge was DILI (n = 29,478) according to the Roussel Uclaf Causality Assessment Method. RESULTS: Most cases of DILI presented with hepatocellular injury (51.39%; 95% confidence interval [CI] 50.76-52.03), followed by mixed injury (28.30%; 95% CI 27.73-28.87) and cholestatic injury (20.31%; 95% CI 19.80-20.82). The leading single classes of implicated drugs were traditional Chinese medicines or herbal and dietary supplements (26.81%) and antituberculosis medications (21.99%). Chronic DILI occurred in 13.00% of the cases and, although 44.40% of the hepatocellular DILI cases fulfilled Hy's Law criteria, only 280 cases (1.08%) progressed to hepatic failure, 2 cases underwent liver transplantation (0.01%), and 102 patients died (0.39%). Among deaths, DILI was judged to have a primary role in 72 (70.59%), a contributory role in 21 (20.59%), and no role in 9 (8.82%). Assuming the proportion of DILI in the entire hospitalized population of China was represented by that observed in the 66 centers where DILI capture was complete, we estimated the annual incidence in the general population to be 23.80 per 100,000 persons (95% CI 20.86-26.74). Only hospitalized patients were included in this analysis, so the true incidence is likely to be higher. CONCLUSIONS: In a retrospective study to determine the incidence and causes of DILI in mainland China, the annual incidence in the general population was estimated to be 23.80 per 100,000 persons; higher than that reported from Western countries. Traditional Chinese medicines, herbal and dietary supplements, and antituberculosis drugs were the leading causes of DILI in mainland China.


Asunto(s)
Causas de Muerte , Enfermedad Hepática Inducida por Sustancias y Drogas/epidemiología , Enfermedad Hepática en Estado Terminal/inducido químicamente , Fallo Hepático Agudo/inducido químicamente , Sistema de Registros , Enfermedad Aguda , Adulto , Distribución por Edad , Anciano , Enfermedad Hepática Inducida por Sustancias y Drogas/diagnóstico , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , China/epidemiología , Enfermedad Crónica , Estudios de Cohortes , Intervalos de Confianza , Enfermedad Hepática en Estado Terminal/epidemiología , Enfermedad Hepática en Estado Terminal/fisiopatología , Femenino , Humanos , Incidencia , Fallo Hepático Agudo/epidemiología , Fallo Hepático Agudo/fisiopatología , Pruebas de Función Hepática , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Medición de Riesgo , Índice de Severidad de la Enfermedad , Distribución por Sexo , Tasa de Supervivencia , Adulto Joven
4.
Tumour Biol ; 37(8): 11311-20, 2016 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-26951515

RESUMEN

Tazarotene-induced gene 3 (TIG3) was first characterized in tazarotene-treated human keratinocytes and identified as a retinoic acid responder gene, an important mediator of antitumor effects by retinoids. In this study, we aim to investigate the inhibitory effect of TIG3 on the growth of liver cancer and explore its underlying mechanism. Human hepatocellular carcinoma (HCC) Hep3B cells were transfected with plasmid GV141 carrying full-length TIG3 complementary DNA (cDNA). The effects of TIG3 on cell proliferation, apoptosis, and migration were determined in vitro. The suppressor effect of TIG3 on tumor growth was evaluated in vivo in a nude mouse HCC model. We observed that TIG3 expression is decreased in the Hep3B cell line as well as primary HCC tumors, and TIG3 expression inversely correlates with Ki-67 expression. Overexpression of TIG3 suppresses tumor growth in HCC both in vitro and in vivo via ERK1/2 inhibition by promoting apoptosis and inhibiting proliferation and migration. These findings identify TIG3 as an attractive therapeutic target for HCC.


Asunto(s)
Carcinoma Hepatocelular/patología , Neoplasias Hepáticas/patología , Sistema de Señalización de MAP Quinasas/fisiología , Receptores de Ácido Retinoico/genética , Adulto , Anciano , Animales , Apoptosis/genética , Western Blotting , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Femenino , Citometría de Flujo , Xenoinjertos , Humanos , Inmunohistoquímica , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Microscopía Confocal , Persona de Mediana Edad , Reacción en Cadena en Tiempo Real de la Polimerasa , Transfección
5.
Dis Colon Rectum ; 49(3): 383-91, 2006 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-16474988

RESUMEN

PURPOSE: This study was designed to investigate the effects and mechanisms of anal electric stimulation with long pulses on anal sphincter pressure in conscious dogs. METHODS: The study was performed after enema in nine healthy female hound dogs and composed of four randomized sessions ("dose"-response, anal electric stimulation only, or with atropine or phentolamine). The anal sphincter pressure was measured by using manometry and quantified by using the area under the contractile curve (mmHg/sec). Anal electric stimulation was performed via a pair of ring electrodes attached to a manometric catheter. The stimulation parameters in all but dose-response sessions included a frequency of 20 ppm, pulse width of 200 ms, and amplitude of 3 mA. RESULTS: The anal sphincter pressure was 55.7 +/- 6 at baseline and increased by 37 percent to 76.4 +/- 6.5 during electric stimulation (P = 0.009). The increase of anal pressure during stimulation was positively correlated with the stimulation energy (r = 0.395; P < 0.01). The excitatory effect of electric stimulation was sustained for at least 20 minutes. Atropine did not alter anal pressure and did not abolish the excitatory effect of anal electric stimulation on the sphincter. Phentolamine reduced anal pressure from the baseline value of 50.5 +/- 4.7 to 33.1 +/- 5.4 (P = 0.019). The electric stimulation induced increase in anal pressure was dropped from 19 +/- 2.6 to 9.9 +/- 2.8 (P = 0.029) at the presence of phentolamine. CONCLUSIONS: Anal electric stimulation with long pulses increases anal sphincter pressure in an energy-dependent manner. The alpha-adrenergic but not the cholinergic pathway at least partially mediates the excitatory effect of anal electric stimulation.


Asunto(s)
Canal Anal/fisiología , Estimulación Eléctrica/métodos , Presión , Antagonistas Adrenérgicos alfa/farmacología , Animales , Atropina/farmacología , Perros , Femenino , Manometría , Antagonistas Muscarínicos/farmacología , Fentolamina/farmacología
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