Exposure to cigarette smoke is an important risk factor for cardiovascular diseases. Nicotine is an addictive compound in cigarette smoke that triggers oxidative stress, which leads to vascular dysfunction. Roxb. is a herb with antioxidant and vascular protective effects. This study evaluated the potential protective effect of the aqueous extract of leaf (AEPS) on vascular dysfunction in rats induced with prolonged nicotine administration. A total of 22 male Sprague-Dawley rats were divided into control (normal saline, oral gavage [p.o.]), nicotine (0.8 mg/kg/day nicotine, intraperitoneally [i.p.]), and nicotine + AEPS groups (250 mg/kg/day AEPS, p.o. + 0.8 mg/kg/day nicotine, i.p.). Treatment was given for 21 days. Thoracic aortae were harvested from the rats for the measurement of vasorelaxation, vascular nitric oxide (NO) level, and antioxidant level and the assessment of vascular remodeling. Rats treated with AEPS had improved vasorelaxation to endothelium-dependent vasodilator, acetylcholine (ACh), compared with the nicotine-induced rats ( < 0.05). The presence of endothelium increased the maximum relaxation of aortic rings in response to ACh. Compared with the nicotine group, AEPS enhanced vascular NO level ( < 0.001) and increased antioxidant levels as measured by superoxide dismutase activity ( < 0.05), catalase activity ( < 0.01), and reduced glutathione level ( < 0.05). No remarkable changes in aortic histomorphometry were detected. In conclusion, attenuates vascular endothelial dysfunction in nicotine-induced rats by improving vasorelaxation and enhancing vascular NO and antioxidant levels.
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http://dx.doi.org/10.3389/fphar.2021.667102 | DOI Listing |
J Clin Periodontol
January 2025
School of Medicine, Tzu Chi University, Hualien, Taiwan, ROC.
Aim: Neurodegenerative diseases are characterized by early increased beta-amyloid (Aβ) and decreased cerebrovascular reactivity. We investigated Aβ in gingiva, serum or hippocampus and neurovascular reactivity in basilar artery (BA) of periodontitis rats, to test the impact of Aβ on BA vasoreactivity ex vivo.
Materials And Methods: Periodontitis was induced in 32 rats using silk-ligation.
Drug Alcohol Depend
December 2024
Department of Psychiatry, University of Florida, Gainesville, FL, USA. Electronic address:
Tobacco use disorder is a chronic disorder that affects more than one billion people worldwide and causes the death of millions each year. The rewarding properties of nicotine are critical for the initiation of smoking. Previous research has shown that the activation of glucocorticoid receptors (GRs) plays a role in nicotine self-administration in rats.
View Article and Find Full Text PDFPol J Vet Sci
December 2024
Technology and Research Research & Development Center (MARGEM), Hatay Mustafa Kemal University, Hatay, Turkey.
Nicotine, the main toxic component of tobacco, directly or indirectly causes adverse effects on the liver metabolism. Melatonin, secreted by the pineal gland, has anti-apoptotic activity as well as antioxidant activity. The aim of this study was to reveal the antiapoptotic effects of melatonin in rats with experimentally induced chronic liver damage with nicotine.
View Article and Find Full Text PDFInt J Prev Med
September 2024
Chronic Respiratory Disease Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background: Nicotine is a behavioral stimulant that in high doses, through the neuro-inflammatory and oxidative stress pathway, can induce apoptosis and autophagy leading to cell death. Previous data indicate that crocin has neuroprotective properties. The aim of the current study is to investigate crocin's neuroprotective effects against nicotine-triggered neuro-inflammation, apoptosis, and autophagy in rat hippocampus.
View Article and Find Full Text PDFToxicology
December 2024
Department of Neurology and Neuroscience, Fujita Health University Hospital, Toyoake, Aichi 470-1192, Japan.
Although cigarette smoking is known to be a critical risk factor for various organ systems and cancers, accumulating evidence indicates that nicotine - a main constituent of cigarette smoking - can exert neuroprotective effects on neuronal cells through nicotinic acetylcholine receptors (nAChRs). However, the precise molecular mechanisms for nicotinic neuroprotective actions remain to be fully elucidated. In this study, we examine the effects of agonists, such as nicotine and PNU282987, on tropomyosin-related kinase (Trk)-dependent neuroprotective pathways in PC12 cells overexpressing a Trk neurotrophin receptor (PCtrk cells).
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