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1.
Neuroscience ; 555: 92-105, 2024 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-39032805

RESUMO

This study utilized network pharmacology and docking analyses to explore a groundbreaking therapeutic approach for managing the neuropathic pain and depressive disorder (NP/DD) comorbidity. Schisandra chinensis (SC), a common Chinese medicine, has demonstrated numerous beneficial effects in treating neuropsychological disorders. The main objective of this study was to identify potential bioactive components of SC and investigate their interactions with relevant target genes associated with NP/DD. To gain insights into the underlying molecular mechanisms, GO and KEGG analyses were conducted. Furthermore, molecular docking analysis was employed to validate the therapeutic relevance of SC's active ingredients. Seven bioactive components of SC, namely Longikaurin A, Deoxyharringtonine, Angeloylgomisin O, Schisandrin B, Gomisin A, Gomisin G, and Gomisin R, exhibited effectiveness in the treatment of NP/DD. From this list, the first five components were selected for further analysis. The analyses revealed a complex network of interactions between the targets of SC and NP/DD, providing valuable information about the molecular mechanisms involved in the treatment of NP/DD with SC. SC components demonstrated the ability to regulate pathways involving tumor necrosis factor (TNF), vascular endothelial growth factor (VEGF), and other growth hormones (GH). Overall, this study contributes to our understanding of the molecular mechanisms underlying the effects of SC in treating NP/DD. Further investigation is necessary to explore the therapeutic potential of SC as a viable strategy for NP/DD comorbidity. These findings lay a solid foundation for future research endeavors in this field, holding potential implications for the development of novel therapeutic interventions targeting NP/DD.


Assuntos
Simulação de Acoplamento Molecular , Farmacologia em Rede , Neuralgia , Schisandra , Schisandra/química , Simulação de Acoplamento Molecular/métodos , Neuralgia/tratamento farmacológico , Neuralgia/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Medicamentos de Ervas Chinesas/uso terapêutico , Humanos , Animais , Depressão/tratamento farmacológico , Comorbidade , Transtorno Depressivo/tratamento farmacológico , Transtorno Depressivo/metabolismo
2.
J Tradit Complement Med ; 10(5): 487-495, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32953565

RESUMO

BACKGROUND: Ethephon (EP) is the most famous plant growth regulator with different adverse effects on kidney function. Virgin Olive Oil (VOO) is considered as a natural source of antioxidant with beneficial effects. Thus, this study was conducted to investigate the effects of VOO on nephrotoxicity induced by EP in rats. METHODS AND MATERIALS: In this study, 80 male rats (weighing 200-250 g) were divided into four groups including I: control group received normal saline as vehicle, II: received VOO, III: received EP (150 mg/kg/day) for 2 months, IV: received EP (150 mg/kg/day for 2 months, after 2-month pretreatment with VOO. VOO (2 mL/kg/day) and vehicle were administered by gastric gavage for 2 months. At the end, the animals were sacrificed, and their blood and kidneys were used for examinations. Isolated kidneys were used for histopathological and oxidative stress studies. RESULTS: Significant increases were recorded in blood (neutrophils, monocytes) and urinary parameters as well as malondialdehyde (MDA) content in the group III compared to groups II and I (P˂0.05). Antioxidant enzymes significantly declined and histopathological alterations increased in the group III. In the group IV, significant decreases were recorded in blood and urinary parameters, MDA, and histopathological alterations and a significant increase were found in antioxidant enzymes compared to group III (P˂0.05). CONCLUSIONS: Findings of the present study demonstrated protective effects of VOO in prevention of kidneys against EP -induced toxicity in albino rats.

3.
Exp Toxicol Pathol ; 65(5): 513-21, 2013 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-22658673

RESUMO

Monosodium glutamate (MSG) is a commonly used food enhancer. Glutamate is used as food additive for enhancing the "meat flavor" of food and gives a particular taste named "umami". In this study, we evaluated the effect of vitamin C on monosodium glutamate induced rat liver injury. This study was divided into 3 groups: group 1 received a diet containing 0.9% NaCl; group 2 received diet containing MSG 6 mg/g/b.w.; and group 3 received a diet containing 6 mg/g/b.w. followed by vitamin C (500 mg/kg/b.w.) for 45 days. The resulting changes were detected using histological, histochemical, ultrastructural, and immuohistochemical analysis. Severe alterations were recorded including dilatations of the central veins; severe cyto-architectural distortions of the hepatocytes; marked reduction in both carbohydrates and proteins; vacuolated cytoplasm, swollen mitochondria and vesiculated rough endoplasmic reticulum with picknotic nuclei; in addition to significant variation in the expression of ki-67 and p53 proteins. The data obtained from this study showed the improvements in the pathological architecture of the liver after treatment with vitamin C. The present data point to the ameliorative effect of vitamin C against MSG induced liver injury.


Assuntos
Antioxidantes/uso terapêutico , Ácido Ascórbico/uso terapêutico , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Fígado/efeitos dos fármacos , Glutamato de Sódio/toxicidade , Animais , Antioxidantes/administração & dosagem , Ácido Ascórbico/administração & dosagem , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Colágeno/metabolismo , Modelos Animais de Doenças , Glicogênio/metabolismo , Imuno-Histoquímica , Antígeno Ki-67/metabolismo , Fígado/metabolismo , Fígado/ultraestrutura , Masculino , Microscopia Eletrônica de Transmissão , Ratos , Proteína Supressora de Tumor p53/metabolismo
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