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Métodos Terapéuticos y Terapias MTCI
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1.
Molecules ; 28(24)2023 Dec 12.
Artículo en Inglés | MEDLINE | ID: mdl-38138535

RESUMEN

Humans are constantly at high risk of emerging pandemics caused by viral and bacterial infections. The emergence of new pandemics is mainly caused by evolved viruses and bacteria that are highly resistant to existing medications. The rapid evolution of infectious agents demands the urgent investigation of new therapeutic strategies to prevent and treat these infections at an early stage. One of these therapeutic strategies includes the use of medicinal herbs for their antibacterial and antiviral properties. The use of herbal medicines as remedies is very ancient and has been employed for centuries. Many studies have confirmed the antimicrobial activities of herbs against various pathogens in vitro and in vivo. The therapeutic effect of medicinal herbs is mainly attributed to the natural bioactive molecules present in these plants such as alkaloids, flavonoids, and terpenoids. Different mechanisms have been proposed for how medicinal herbs enhance the immune system and combat pathogens. Such mechanisms include the disruption of bacterial cell membranes, suppression of protein synthesis, and limitation of pathogen replication through the inhibition of nucleic acid synthesis. Medicinal herbs have been shown to treat a number of infectious diseases by modulating the immune system's components. For instance, many medicinal herbs alleviate inflammation by reducing pro-inflammatory cytokines (e.g., tumor necrosis factor-alpha (TNF-α), interleukin-1, IL-6) while promoting the production of anti-inflammatory cytokines (e.g., IL-10). Medicinal herbs also play a role in defense against viral and intracellular infections by enhancing the proliferation and functions of natural killer cells, T-helper-1 cells, and macrophages. In this review, we will explore the use of the most common herbs in preventing and treating infectious and non-infectious diseases. Using current and recently published studies, we focus on the immunomodulatory and therapeutic effects induced by medicinal herbs to enhance immune responses during diseases.


Asunto(s)
Enfermedades Transmisibles , Plantas Medicinales , Humanos , Plantas Medicinales/metabolismo , Fitoterapia , Factores Inmunológicos/farmacología , Factores Inmunológicos/uso terapéutico , Citocinas/metabolismo , Enfermedades Transmisibles/tratamiento farmacológico , Adyuvantes Inmunológicos
2.
Int J Mol Sci ; 24(18)2023 Sep 06.
Artículo en Inglés | MEDLINE | ID: mdl-37762060

RESUMEN

Type 2 diabetes (T2D) is a chronic metabolic condition associated with obesity, oxidative stress-mediated inflammation, apoptosis, and impaired insulin signaling. The utilization of phytochemical therapy generated from plants has emerged as a promising approach for the treatment of diabetes and its complications. Kiwifruit is recognized for its substantial content of antioxidative phenolics. Therefore, this work aimed to examine the effect of Actinidia deliciosa (kiwi fruit) on hepatorenal damage in a high-fat diet (HFD) and streptozotocin (STZ)-induced T2D in rats using in vivo and in silico analyses. An increase in hepatic and renal lipid peroxidation was observed in diabetic rats accompanied by a decrease in antioxidant status. Furthermore, it is important to highlight that there were observable inflammatory and apoptotic responses in the hepatic and renal organs of rats with diabetes, along with a dysregulation of the phosphorylation levels of mammalian target of rapamycin (mTOR), protein kinase B (Akt), and phosphoinositide 3-kinase (PI3K) signaling proteins. However, the administration of kiwi extract to diabetic rats alleviated hepatorenal dysfunction, inflammatory processes, oxidative injury, and apoptotic events with activation of the insulin signaling pathway. Furthermore, molecular docking and dynamic simulation studies revealed quercetin, chlorogenic acid, and melezitose as components of kiwi extract that docked well with potential as effective natural products for activating the silent information regulator 1(SIRT-1) pathway. Furthermore, phenolic acids in kiwi extract, especially syringic acid, P-coumaric acid, caffeic acid, and ferulic acid, have the ability to inhibit the phosphatase and tensin homolog (PTEN) active site. In conclusion, it can be argued that kiwi extract may present a potentially beneficial adjunctive therapy approach for the treatment of diabetic hepatorenal complications.


Asunto(s)
Actinidia , Complicaciones de la Diabetes , Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 2 , Insulinas , Animales , Ratas , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Diabetes Mellitus Experimental/complicaciones , Diabetes Mellitus Experimental/tratamiento farmacológico , Simulación del Acoplamiento Molecular , Fosfatidilinositol 3-Quinasas , Antioxidantes , Extractos Vegetales/farmacología , Extractos Vegetales/uso terapéutico , Mamíferos
3.
Oxid Med Cell Longev ; 2022: 4812993, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36304965

RESUMEN

Neuroinflammation is documented to alter brain function as a consequence of metabolic changes linked with a high-fat diet (HFD). The primary target of this study is to see how geraniol is effective in manipulating age- and diet-associated multiple toxicity and neuroinflammation in HFD-fed rats. Sixty-four adult male Wistar rats were partitioned into two groups: Group 1 (untreated normal young and aged rats) and Group 2 (HFD-fed young and aged rats) that received HFD for 16 weeks before being orally treated with geraniol or chromax for eight weeks. The results revealed a dropping in proinflammatory cytokines (TNF-α and IL-6) and leptin while boosting adiponectin in geraniol-supplemented rats. The liver, kidney, and lipid profiles were improved in geraniol-HFD-treated groups. HFD-induced brain insulin resistance decreased insulin clearance and insulin-degrading enzyme (IDE) levels significantly after geraniol supplementation. Geraniol suppressed acetylcholinesterase (AChE) activity and alleviated oxidative stress by boosting neuronal reduced glutathione (GSH), catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities. It lowered malondialdehyde concentration (TBARS), nitric oxide (NO), and xanthine oxidase (XO) and restored the structural damage to the brain tissue caused by HFD. Compared with model rats, geraniol boosted learning and memory function and ameliorated the inflammation status in the brain by lowering the protein levels of IL-1ß, iNOS, NF-κBp65, and COX-2. In addition, the expression levels of inflammation-related genes (MCP-1, TNF-α, IL-6, IL-1ß, and IDO-1) were lessened significantly. Remarkably, the supplementation of geraniol reversed the oxidative and inflammation changes associated with aging. It affected the redox status of young rats. In conclusion, our results exhibit the effectiveness of dietary geraniol supplementation in modifying age-related neuroinflammation and oxidative stress in rats and triggering off the use of geraniol as a noninvasive natural compound for controlling age- and diet-associated neuronal impairments and toxicity.


Asunto(s)
Dieta Alta en Grasa , Factor de Necrosis Tumoral alfa , Ratas , Masculino , Animales , Dieta Alta en Grasa/efectos adversos , Factor de Necrosis Tumoral alfa/metabolismo , Acetilcolinesterasa/metabolismo , Interleucina-6/metabolismo , Estudios Prospectivos , Ratas Wistar , Inflamación/tratamiento farmacológico , Inflamación/metabolismo , Estrés Oxidativo
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