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1.
Molecules ; 27(23)2022 Dec 06.
Article in English | MEDLINE | ID: mdl-36500700

ABSTRACT

The present study investigated the cardioprotective properties of 6-gingerol against alcohol-induced ROS-mediated cardiac tissue damage in rats. Experiments were conducted on 4 groups of rats, orally treated with control, 6-gingerol (10 mg/kg body weight), alcohol (6 g/kg body weight) and combination of 6-gingerol plus alcohol for two-month. In the results, we found 6-ginger treatment to alcohol-fed rats substantially suppressed ROS production in cardiac tissue. Alcohol-induced elevated 8-OHDG and protein carbonyls which represent oxidative modification of DNA and proteins were completely reversed by 6-gingerol. This was further endorsed by restored superoxide dismutase and catalase activities with 6-gingerol against alcohol-induced loss. The elevated cardiac biomarkers (CK-MB, cTn-T, cTn-I) and dyslipidemia in alcohol-intoxicated rats was significantly reversed by 6-gingerol. Furthermore, alcohol-induced apoptosis characterized by overexpression of cytochrome C, caspase-8 and caspase-9 was diminished with 6-gingerol treatment. Transmission electron microscope images conferred the cardioprotective properties of 6-gingerol as we have seen less structural derangements in mitochondria and reappearance of myofilaments. Our findings conclude that 6-ginger effectively protect alcohol-induced ROS-mediated cardiac tissue damage, which may be due to its potent antioxidant efficacy. Therefore, 6-gingerol could be a potential therapeutic molecule that can be used in the treatment of alcohol-induced myocardial injury.


Subject(s)
Oxidative Stress , Zingiber officinale , Rats , Animals , Fatty Alcohols/pharmacology , Fatty Alcohols/chemistry , Catechols/pharmacology , Catechols/chemistry , Apoptosis , Zingiber officinale/chemistry , Antioxidants/pharmacology , Antioxidants/metabolism , Body Weight
2.
Molecules ; 26(20)2021 Oct 15.
Article in English | MEDLINE | ID: mdl-34684831

ABSTRACT

In our in vitro and in vivo studies, we used Acalypha indica root methanolic extract (AIRME), and investigated their free radical scavenging/antioxidant and anti-inflammatory properties. Primarily, phytochemical analysis showed rich content of phenols (70.92 mg of gallic acid/g) and flavonoids (16.01 mg of rutin/g) in AIRME. We then performed HR-LC-MS and GC-MS analyses, and identified 101 and 14 phytochemical compounds, respectively. Among them, ramipril glucuronide (1.563%), antimycin A (1.324%), swietenine (1.134%), quinone (1.152%), oxprenolol (1.118%), choline (0.847%), bumetanide (0.847%) and fenofibrate (0.711%) are the predominant phytomolecules. Evidence from in vitro studies revealed that AIRME scavenges DPPH and hydroxyl radicals in a concentration dependent manner (10-50 µg/mL). Similarly, hydrogen peroxide and lipid peroxidation were also remarkably inhibited by AIRME as concentration increases (20-100 µg/mL). In vitro antioxidant activity of AIRME was comparable to ascorbic acid treatment. For in vivo studies, carrageenan (1%, sub-plantar) was injected to rats to induce localized inflammation. Acute inflammation was represented by paw-edema, and significantly elevated (p < 0.05) WBC, platelets and C-reactive protein (CRP). However, AIRME pretreatment (150/300 mg/kg bodyweight) significantly (p < 0.05) decreased edema volume. This was accompanied by a significant (p < 0.05) reduction of WBC, platelets and CRP with both doses of AIRME. The decreased activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase in paw tissue were restored (p < 0.05 / p < 0.01) with AIRME in a dose-dependent manner. Furthermore, AIRME attenuated carrageenan-induced neutrophil infiltrations and vascular dilation in paw tissue. For the first time, our findings demonstrated the potent antioxidant and anti-inflammatory properties of AIRME, which could be considered to develop novel anti-inflammatory drugs.


Subject(s)
Acalypha/chemistry , Phytochemicals/chemistry , Phytochemicals/pharmacology , Plants, Medicinal/chemistry , Animals , Anti-Inflammatory Agents/chemistry , Anti-Inflammatory Agents/pharmacology , Antioxidants/chemistry , Antioxidants/pharmacology , Disease Models, Animal , Edema/drug therapy , Edema/enzymology , Edema/pathology , Free Radical Scavengers/chemistry , Free Radical Scavengers/pharmacology , In Vitro Techniques , Male , Phytotherapy , Plant Extracts/chemistry , Plant Extracts/pharmacology , Plant Roots/chemistry , Rats , Rats, Wistar
3.
Curr Pharm Des ; 26(39): 4955-4969, 2020.
Article in English | MEDLINE | ID: mdl-32744961

ABSTRACT

BACKGROUND: The prevalence of diabetes in the world population hás reached 8.8 % and is expected to rise to 10.4% by 2040. Hence, there is an urgent need for the discovery of drugs against therapeutic targets to sojourn its prevalence. Previous studies proved that NF-κB serves as a central agent in the development of diabetic complications. OBJECTIVES: This review intended to list the natural plant compounds that would act as inhibitors of NF-κB signalling in different organs under the diabetic condition with their possible mechanism of action. METHODS: Information on NF-κB, diabetes, natural products, and relation in between them, was gathered from scientific literature databases such as Pubmed, Medline, Google scholar, Science Direct, Springer, Wiley online library. RESULTS AND CONCLUSION: NF-κB plays a crucial role in the development of diabetic complications because of its link in the expression of genes that are responsible for organs damage such as kidney, brain, eye, liver, heart, muscle, endothelium, adipose tissue and pancreas by inflammation, apoptosis and oxidative stress. Activation of PPAR-α, SIRT3/1, and FXR through many cascades by plant compounds such as terpenoids, iridoids, flavonoids, alkaloids, phenols, tannins, carbohydrates, and phytocannabinoids recovers diabetic complications. These compounds also exhibit the prevention of NF-κB translocation into the nucleus by inhibiting NF-κB activators, such as VEGFR, RAGE and TLR4 receptors, which in turn, prevent the activation of many genes involved in tissue damage. Current knowledge on the treatment of diabetes by targeting NF-κB is limited, so future studies would enlighten accordingly.


Subject(s)
Diabetes Complications , Diabetes Mellitus, Experimental , Animals , Humans , Inflammation/drug therapy , NF-kappa B/metabolism , Oxidative Stress
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