Molecular basis of vascular damage caused by cigarette smoke exposure and a new approach to the treatment: Alpha-linolenic acid

Kaplan, Halil Mahir; Kuyucu, Yurdun; Polat, Sait; Pazarcı, Perçin; Yegani, Arash Alizadeh; Şingirik, Ergin; Ertuğ, Peyman U.

doi:10.1016/j.biopha.2018.03.112

Cited by 10 publications

(4 citation statements)

References 27 publications

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“…In addition, ALA (40.74% of the diet) protected the vascular endothelial function of HFD‐induced rats by promoting the production of constitutive NO (Hermier et al, 2016). Kaplan et al (2018) also found that ALA (200 mg/kg) improved the smooth muscle damage of the rat thoracic aorta caused by smoking by inhibiting the expression of COX‐2 and PLA 2 and increasing the expression of eNOS. In short, ALA can protect the vascular endothelial function and prevent the occurrence of atherosclerosis by inhibiting the inflammatory response and the production of foam cells.…”

Section: Pharmacological Effectsmentioning

confidence: 96%

The review of alpha‐linolenic acid: Sources, metabolism, and pharmacology

Yuan

Xie

Huang

et al. 2021

Phytotherapy Research

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α‐linolenic acid (ALA, 18:3n‐3) is a carboxylic acid composed of 18 carbon atoms and three cis double bonds, and is an essential fatty acid indispensable to the human body. This study aims to systematically review related studies on the dietary sources, metabolism, and pharmacological effects of ALA. Information on ALA was collected from the internet database PubMed, Elsevier, ResearchGate, Web of Science, Wiley Online Library, and Europe PMC using a combination of keywords including “pharmacology,” “metabolism,” “sources.” The following findings are mainly contained. (a) ALA can only be ingested from food and then converted into eicosapentaenoic acid and docosahexaenoic acid in the body. (b) This conversion process is relatively limited and affected by many factors such as dose, gender, and disease. (c) Pharmacological research shows that ALA has the anti‐metabolic syndrome, anticancer, antiinflammatory, anti‐oxidant, anti‐obesity, neuroprotection, and regulation of the intestinal flora properties. (d) There are the most studies that prove ALA has anti‐metabolic syndrome effects, including experimental studies and clinical trials. (e) The therapeutic effect of ALA will be affected by the dosage. In short, ALA is expected to treat many diseases, but further high quality studies are needed to firmly establish the clinical efficacy of ALA.

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Section: Pharmacological Effectsmentioning

confidence: 96%

The review of alpha‐linolenic acid: Sources, metabolism, and pharmacology

Yuan

Xie

Huang

et al. 2021

Phytotherapy Research

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“…Vascular endothelium cells (VEC) play a fundamental role in the human body; ensuring the regulation of vasomotor functions, the maintenance of vessel walls, anti-platelet aggregation, and endocrine functions. Numerous harmful stimuli can lead to endothelial cell dysfunction (ECD) with consequential increases in the risk of many diseases including cardiovascular diseases (Vykoukal and Davies, 2011;Khaddaj Mallat et al, 2017; Kaplan et al, 2018;Maiuolo et al, 2020a). In MetS patients, the ECD is a specific early pathophysiological indicator of cardiovascular disorders; its recognition and early intervention are of extreme importance in the prevention, treatment, and prognosis of cardiovascular diseases (Wei et al, 2014;Dalal et al, 2020).…”

Section: The Role Of the Endothelium In Metabolic Syndromementioning

confidence: 99%

From Metabolic Syndrome to Neurological Diseases: Role of Autophagy

Maiuolo

Gliozzi

Musolino

et al. 2021

Front. Cell Dev. Biol.

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Metabolic syndrome is not a single pathology, but a constellation of cardiovascular disease risk factors including: central and abdominal obesity, systemic hypertension, insulin resistance (or type 2 diabetes mellitus), and atherogenic dyslipidemia. The global incidence of Metabolic syndrome is estimated to be about one quarter of the world population; for this reason, it would be desirable to better understand the underlying mechanisms involved in order to develop treatments that can reduce or eliminate the damage caused. The effects of Metabolic syndrome are multiple and wide ranging; some of which have an impact on the central nervous system and cause neurological and neurodegenerative diseases. Autophagy is a catabolic intracellular process, essential for the recycling of cytoplasmic materials and for the degradation of damaged cellular organelle. Therefore, autophagy is primarily a cytoprotective mechanism; even if excessive cellular degradation can be detrimental. To date, it is known that systemic autophagic insufficiency is able to cause metabolic balance deterioration and facilitate the onset of metabolic syndrome. This review aims to highlight the current state of knowledge regarding the connection between metabolic syndrome and the onset of several neurological diseases related to it. Furthermore, since autophagy has been found to be of particular importance in metabolic disorders, the probable involvement of this degradative process is assumed to be responsible for the attenuation of neurological disorders resulting from metabolic syndrome.

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“…Having very low side effect profile and possessing considerable and interesting roles as nutrition supplement herbal antioxidant usage has become a popular subject nowadays. In a recent study by Kaplan et al [12], endothelial dysfunction and inflammation that occurs in the thoracic aorta of the mice secondarily after being exposed to cigarette smoke were attempted to neutralize with alpha linolenic acid which is present in flaxseed and soy; as a result alpha-linolenic acid was proven to inhibit the inflammatory mechanisms and prevent the smooth muscle damage caused by cigarette smoking. Nigella sativa L. that belongs to the Ranunculaceae family is a 20-30 cm plant with flowers and its habitat comprises Southwest Asia, North Africa and Europe.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of thymoquinone on smoking-induced vascular damage: An experimental study in rats

Velioğlu

Yüksel

Yakşi

et al. 2019

j-ebr

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To investigate the protective effect of thymoquinone on smoking-induced vascular damage in rats. Method: A total of 28 rats were allocated in this experimental study. Rats were equally divided in four groups; as control group (n=7) and study groups including only smoking group (n=7), smoking plus thymoquinone group (n=7) and smoking plus dexamethasone group (n=7). The animals in study groups were subjected to regular cigarette smoke exposure during 2 months, hereby smoking-induced vascular injury model was established in the animals. The thoracic aorta of the animals were surgically resected and then evaluated histopathologically. The prepared aortic tissue samples were analyzed under light microscope in terms of thickness of aortic wall, endothelial continuity and injury as well as degenerative alterations on the endothelium. Results: Mean aortic wall thicknesses were 77.8 and 114.5 μ in only smoking group and smoking plus thymoquinone group respectively, and this difference was statistically significant. In only smoking group partial endothelial damage and complete endothelial damage were observed in 2 and 4 animals respectively whereas in smoking plus thymoquinone group no endothelial damage and partial endothelial damage were observed in 2 and 4 animals respectively. When these groups were compared in terms of endothelial damage, the difference was detected to be statistically significant. Conclusion:Our study demonstrates that thymoquinone has a protective effect on rat endothelium and alleviates the smoking-induced vascular damage in rats.

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Molecular basis of vascular damage caused by cigarette smoke exposure and a new approach to the treatment: Alpha-linolenic acid

Cited by 10 publications

References 27 publications

The review of alpha‐linolenic acid: Sources, metabolism, and pharmacology

The review of alpha‐linolenic acid: Sources, metabolism, and pharmacology

From Metabolic Syndrome to Neurological Diseases: Role of Autophagy

Protective effect of thymoquinone on smoking-induced vascular damage: An experimental study in rats

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