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... the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). After 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). ...
Context 2
... the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). After 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). In the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). ...
Context 3
... the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). After 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). In the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). ...
Context 4
... 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). In the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). After 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). ...
Context 5
... the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). After 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). ...
Context 6
... the absence of treatment, hypercaloric diet (AAB + HD group) induced an increase in abdominal adipose tissue (Table 2) and plasma leptin and adiponectin (Figure 8a,b) concentrations compared to groups fed with standard diet (AAB + SD and Control). After 36 weeks, the chronic-discontinuous treatment with ALA was able to significantly reduce both abdominal adipose tissue (Table 2) and circulating leptin and adiponectin levels (Figure 8a,b), while significantly increasing adiponectin/leptin ratio (Figure 8c). ...
Context 7
... the end of the study (W36), in the three groups with abdominal aortic stenosis (AAB + SD, AAB + HD and AAB + HD + ALA), plasma levels of Brain Natriuretic Peptide (BNP) and Angiotensin II were significantly lower than the values obtained in the Control group (Figure 10a,b). The chronic-discontinuous treatment with ALA did not influence plasma BNP concentration ( Figure Figure 8. Adiposity markers: (a) Leptin, (b) Adiponectin and (c) Adiponectin/leptin ratio (one-factor ANOVA). ...
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https://meddocsonline.org/annals-of-cardiology-and-vascular-medicine/atrial-fibrillation-in-heart-failure-with-preserved-ejection-fraction.pdf
Citations
... α-lipoic acid (1,2-dithiolane-3-pentanoic acid) is a sulfur containing vitamin-like compound gaining popularity as a nutritional supplement to combat obesity and age-associated complications (Shay et al., 2009;Park et al., 2014;Salehi et al., 2019). Discontinuous treatment of Sprague-Dawley rats with α-lipoic acid at 50 mg/kg body weight prevented gain in body weight and had a protective e cacy on the cardiovascular system by decreasing metabolic and cardiac perturbations (Pop et al., 2020). In another study, chronic treatment of diet induced obese mice with 250 mg/kg of α-lipoic acid in combination with β3-AR agonist CL 316,243 improved body mass composition, reduced body fat percentage by 9% and improved systemic and epididymal white adipose tissue in ammation (Abdul Sater et al., 2022). ...
Consumption of a high fat diet is accompanied with the risk of obesity and early onset of age-associated complications. Hence, dietary interventions are imperative to combat this. α-lipoic acid has been shown to hinder diet-induced obesity in model organisms. Recent studies hint at probable lifespan extending efficacy of α-lipoic acid as well. Drosophila melanogaster has emerged as a robust model organism for longevity studies. In this study, α-lipoic acid was investigated for its efficacy to improve lifespan and age-associated physiology in Canton-S strain of Drosophila melanogaster fed with a high fat diet. Furthermore, as mating status has a significant impact on survival in fruit-flies, flies were reared in two experimental groups – group one in which males and females were reared together and group two in which males and females were reared separately. In group one, α-lipoic acid improved mean lifespan, reduced fecundity of females and reduced mean body weight of flies at dose range of 2mM – 2.5mM, respectively. In group two, α-lipoic acid improved mean lifespan, reduced fecundity of females and reduced mean body weight of flies at dose range of 1mM – 2.5mM, respectively. Improved climbing efficiency was observed with α-lipoic acid at dose range of 1.5mM – 2.5mM in flies of group one and 1mM – 2.5mM in flies of group two, respectively. Administration of α-lipoic acid improved resistance to oxidative stress in only female flies of group one at 2.5mM whereas in group two, both male and female flies exhibited improved resistance to oxidative stress with α-lipoic acid at dose range of 2mM – 2.5mM, respectively. Male and female flies of only group one showed improved resistance to heat shock stress with α-lipoic acid at dose range of 2mM – 2.5mM. Only female flies of group two exhibited a small significant improvement in recovery time following cold shock with α-lipoic acid only at 2.5mM. No significant change in resistance to starvation stress was observed with any dose of α-lipoic acid in either group of flies. To summarize, data from this study suggested a probable dose and gender dependent efficacy of α-lipoic acid in flies fed with a high fat diet; this efficacy was also significantly impacted by mating status of flies due to varied rearing conditions.
... However, we also found during the development and treatment of CHF, compared with normal group, the expression levels of Cyt-C and AIF in rats in model group, moxibustion group, benazepril group and aibei group were increased, indicating the excessive apoptosis of cardiomyocytes caused by Cyt-C and AIF might be the important reasons for CHF. Because of the slow onset and long course of CHF, CHF is often accompanied by left ventricular remodeling and functional impairment, accompanied by the decrease of EF, FS, CO and LVSP, the increase of SV and LVEDP, and the acceleration of HR. 35,36 In addition, there will be swelling of cardiomyocytes, hyperchromatism of nuclei, alteration of cytoplasmic vacuolation, rupture and dissolution of myocardial fibers as well as disordered arrangement in myocardial tissues. 36 In this experiment, after treatment, EF, FS, CO and LVSP in CHF rats were increased, while SV, HR and LVEDP were decreased, myocardial cells in moxibustion group, benazepril group and aibei group were dyed evenly, and the muscle fibers were arranged neatly, indicating that CHF rat cardiac function was improved after treatment. ...
Objective:
To observe the effects of moxibustion at bilateral Feishu (BL13) and Xinshu (BL15) combined with benazepril on myocardial cells apoptosis index, the expression levels of apoptosis-related proteins cytochrome c (Cyt-C) and apoptosis-inducing factor (AIF) in chronic heart failure (CHF) rats.
Methods:
Sixty-five rats were randomly divided into normal group () and model-I group (). After modeling, CHF rats in model-I group were divided into model group, moxibustion group, benazepril group, moxibustion plus benazepril group (abbreviated as aibei group, the same below), 10 rats in each group. Echocardiogram index was examined by echocardiography. Hemodynamic indices were measured by rat cardiac function meter. Serum B-type brain natriuretic peptide (BNP) was detected by enzyme-linked immunosorbent assay. Myocardial cells apoptosis index was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling staining. Pathological changes of myocardial tissues were observed by hematoxylin and eosin staining. The expression levels of Cyt-C and AIF in myocardial tissues were detected by Western blot.
Results:
Compared with normal group, ejection fraction and left ventricular diameter shortening rate in model-Ⅰ group were significantly reduced, myocardial cells of rats in model group exhibited unclear transverse striations, cells swellings and vacuoles, cardiac functions were deteriorated, serum BNP level, myocardial cells apoptosis index, and the expression levels of Cyt-C and AIF were significantly increased. Compared with model group, myocardial cells of rats in moxibustion group, benazepril group, and aibei group were dyed more evenly, muscle fibers were arranged relatively neatly, cardiac functions were improved, serum BNP level, myocardial cells apoptosis index, and the expression levels of Cyt-C and AIF were significantly decreased. Compared with aibei group, cardiac functions were worsened, myocardial cells apoptosis index, and the expression levels of Cyt-C and AIF were increased.
Conclusion:
Moxibustion at bilateral Feishu (BL13) and Xinshu (BL15) combined with benazepril could improve CHF better than moxibustion at bilateral Feishu (BL13) and Xinshu (BL15) or benazepril alone. The mechanisms might be that they can inhibit the expressions of Cyt-C and AIF, and inhibit the apoptosis of cardiomyocytes.
... Moreover, in the last few years, ALA has exceeded the status of antioxidant, its ability to mediate and regulate multiple signaling pathways having been demonstrated. Thus, besides its use as adjuvant therapy for diabetic neuropathy in some European countries, multiple studies have reported the benefits of ALA treatment in metabolic disorders (hyperglycemia, tissue insulin resistance, dyslipidemia or obesity) [59][60][61], endothelial dysfunction [62][63][64][65] or in various inflammatory processes [63,66]. Another great advantage of ALA is represented by its amphiphilic properties, due to which ALA can be distributed both in hydrophilic (plasma, cell cytoplasm, etc.) and in lipophilic (cell membranes, etc.) environments. ...
... Due to the low cytokine levels and by inducing heme oxygenase-1 upregulation, ALA subsequently decreases the adhesion molecules' expression (E-selectine, vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1)) and the extravascular leucocyte migration (Figure 2a) [98,113]. A significant number of recent clinical trials [63,66,114] and experimental studies [60,61] have reported the efficacy of ALA in different inflammatory process by decreasing the inflammatory markers such us CRP, IL-6 or TNF-α [115]. In this context, it was noted that ALA contributes to multiple organ protection in sepsis [115], in part through activation of autophagy, too [116]. ...
Coronavirus disease 2019 (COVID-19) was first reported in Wuhan, China, in late December 2019. Since then, COVID-19 has spread rapidly worldwide and was declared a global pandemic on 20 March 2020. Cardiovascular complications are rapidly emerging as a major peril in COVID-19 in addition to respiratory disease. The mechanisms underlying the excessive effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on patients with cardiovascular comorbidities remain only partly understood. SARS-CoV-2 infection is caused by binding of the viral surface spike (S) protein to the human angiotensin-converting enzyme 2 (ACE2), followed by the activation of the S protein by transmembrane protease serine 2 (TMPRSS2). ACE2 is expressed in the lung (mainly in type II alveolar cells), heart, blood vessels, small intestine, etc., and appears to be the predominant portal to the cellular entry of the virus. Based on current information, most people infected with SARS-CoV-2 virus have a good prognosis, while a few patients reach critical condition, especially the elderly and those with chronic underlying diseases. The “cytokine storm” observed in patients with severe COVID-19 contributes to the destruction of the endothelium, leading to “acute respiratory distress syndrome” (ARDS), multiorgan failure, and death. At the origin of the general proinflammatory state may be the SARS-CoV-2-mediated redox status in endothelial cells via the upregulation of ACE/Ang II/AT1 receptors pathway or the increased mitochondrial reactive oxygen species (mtROS) production. Furthermore, this vicious circle between oxidative stress (OS) and inflammation induces endothelial dysfunction, endothelial senescence, high risk of thrombosis and coagulopathy. The microvascular dysfunction and the formation of microthrombi in a way differentiate the SARS-CoV-2 infection from the other respiratory diseases and bring it closer to cardiovascular diseases like myocardial infarction and stroke. Due the role played by OS in the evolution of viral infection and in the development of COVID-19 complications, the use of antioxidants as adjuvant therapy seems appropriate in this new pathology. Alpha-lipoic acid (ALA) could be a promising candidate that, through its wide tissue distribution and versatile antioxidant properties, interferes with several signaling pathways. Thus, ALA improves endothelial function by restoring the endothelial nitric oxide synthase activity and presents an anti-inflammatory effect dependent or independent of its antioxidant properties. By improving mitochondrial function, it can sustain the tissues’ homeostasis in critical situation and by enhancing the reduced glutathione it could indirectly strengthen the immune system. This complex analysis could open a new therapeutic perspective for ALA in COVID-19 infection.
