RESUMEN
Doxorubicin (DOX), an anthracycline antineoplastic candidate is used to treat various malignancies. Around 41% of patients undergoing DOX treatment develop acute cardiotoxicity. Preventing DOX-induced cardiac fibrosis and hypertrophy helps in evading cardiac remodeling leading to cardiomyopathy and heart failure. Neferine, an alkaloid from the lotus has numerous pharmacological activities. The present study was designed to evaluate the protective effect of neferine on DOX-mediated fibrosis and hypertrophy. DOX-induced fibrosis involves activation of transforming growth factor-ß1 (TGF-ß1), matrix metalloproteinase 2 (MMP-2), and MMP-9 with concomitant downregulation of tissue inhibitors of MMPs (TIMP)-1 and TIMP-2 expressions in H9c2 cardiomyoblasts. Furthermore, DOX treatment also resulted in hypertrophy with the increased cell volume and overexpression of hypertrophy markers calcineurin, brain natriuretic peptide, and atrial natriuretic peptide. Finally, DOX treatment resulted in apoptosis through activation of p53. Pretreatment with neferine markedly activated SIRT1 expression and modulated the expression levels of TGF-ß1 and p53, thereby significantly reducing DOX-induced fibrosis, hypertrophy, and apoptosis in H9c2 cardiomyoblasts.
Asunto(s)
Metaloproteinasa 2 de la Matriz , Factor de Crecimiento Transformador beta1 , Antibióticos Antineoplásicos/farmacología , Apoptosis , Bencilisoquinolinas , Cardiotoxicidad/metabolismo , Doxorrubicina/efectos adversos , Fibrosis , Humanos , Hipertrofia/metabolismo , Hipertrofia/patología , Metaloproteinasa 2 de la Matriz/metabolismo , Miocitos Cardíacos/metabolismo , Factor de Crecimiento Transformador beta1/metabolismo , Proteína p53 Supresora de Tumor/metabolismoRESUMEN
Neurodegenerative diseases are normally distinguished as disorders with loss of neurons. Various compounds are being tested to treat neurodegenerative diseases (NDs) but they possess solitary symptomatic advantages with numerous side effects. Accumulative studies have been conducted to validate the benefit of phytochemicals to treat neurodegenerative diseases including Alzheimer's disease (AD) and Parkinson's disease (PD). In this present review we explored the potential efficacy of phytochemicals such as epigallocatechin-3-galate, berberin, curcumin, resveratrol, quercetin and limonoids against the most common NDs, including Alzheimer's disease (AD) and Parkinson's disease (PD). The beneficial potentials of these phytochemicals have been demonstrated by evidence-based but more extensive investigation needs to be conducted for reducing the progression of AD and PD.
Asunto(s)
Enfermedad de Alzheimer/tratamiento farmacológico , Fármacos Neuroprotectores , Enfermedad de Parkinson/tratamiento farmacológico , Fitoquímicos , Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/patología , Animales , Humanos , Fármacos Neuroprotectores/química , Fármacos Neuroprotectores/uso terapéutico , Enfermedad de Parkinson/metabolismo , Enfermedad de Parkinson/patología , Fitoquímicos/química , Fitoquímicos/uso terapéuticoRESUMEN
Long non coding RNAs (lncRNAs) are involved in modulating the expression of other non-coding RNAs (ncRNA), such as microRNAs, or target proteins through the epigenetic, transcriptional, or post-transcriptional regulations. Genomic mutations in cancer reside inside regions that do not code for proteins and these regions are often transcribed into long non coding RNAs (lncRNAs). Emerging evidences have revealed an intense involvement of lncRNAs in the cancer development and progression. Recently, emerging evidences have depicted that the phytochemicals interact with lncRNAs to modulate their activities. Such findings are highly important for the identification of therapeutic strategies against diseases that are particularly associated with an aberrant lncRNA signaling. This review aims at deciphering the role of lncRNAs in the cancer development and progression, and their regulation by various phytochemicals.
Asunto(s)
Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Invasividad Neoplásica/diagnóstico , Neoplasias/prevención & control , Fitoquímicos/farmacología , ARN Largo no Codificante/fisiología , Humanos , Invasividad Neoplásica/genética , Neoplasias/genética , ARN Largo no Codificante/genéticaRESUMEN
<p><b>OBJECTIVE</b>To assess the effect of quercetin (flavonoid) against lindane induced alterations in lipid profile of wistar rats.</p><p><b>METHODS</b>Rats were administered orally with lindane (100 mg/kg body weight) and quercetin (10 mg/kg body weight) for 30 days. After the end of treatment period lipid profile was estimated in serum and tissue.</p><p><b>RESULTS</b>Elevated levels of serum cholesterol, triglycerides, low density lipoprotein (LDL), very Low Density Lipoprotein (VLDL) and tissue triglycerides, cholesterol with concomitant decrease in serum HDL and tissue phospholipids were decreased in lindane treated rats were found to be significantly decreased in the quercetin and lindane co-treated rats.</p><p><b>CONCLUSIONS</b>Our study suggests that quercetin has hypolipidemic effect and offers protection against lindane induced toxicity in liver by restoring the altered levels of lipids. The quercetin cotreatment along with lindane for 30 days reversed these biochemical alterations in lipids induced by lindane.</p>