scholarly journals Prophylactic Application of Lavandula Angustifolia Mill. Oil and Its Active Component Linalyl Acetate Alleviate Comorbidity and Exacerbation Risk in Rats With Collagen-Induced Arthritis Accompanied by Chronic Nicotine-Induced Hypertension.

Author(s):  
Eunhye Seo ◽  
Yu Shan Hsieh ◽  
Jeong-Min Lee ◽  
You Kyoung Shin ◽  
Geun Hee Seol

Abstract Background: Hypertension (HTN) in rheumatoid arthritis (RA) is more common in smokers than in non-smokers, increasing the risks of cardiovascular and skeletal muscle related comorbidities, but studies on pharmacological protection strategies are insufficient. Lavandula angustifolia Mill. (lavender) oil has traditionally been used for RA and HTN via its anti-inflammatory properties. This study aimed to investigate the effects of lavender oil and its main component linalyl acetate on cardiovascular and skeletal muscle protection in a rat model of RA with chronic nicotine-induced HTN. Methods: Collagen-induced arthritis (CIA), with or without chronic nicotine-induced HTN, were induced in Sprague-Dawley rats. Lavender or linalyl acetate (10 or 100 mg/kg/day) were administrated intraperitoneally to CIA plus chronic nicotine-induced HTN (H-CIA) rats. The effects of lavender and linalyl acetate was evaluated by measurement of hind paw thickness, body weight, blood pressure (BP), serum concentrations of interleukin-6 (IL-6) and insulin-like growth factor-1 (IGF-1). In addition to above, histological analysis of thoracic aorta and gastrocnemius muscle were used. Results: BP was significantly higher, vascular endothelium more deteriorated and paw edema more severe in H-CIA than in CIA. Both groups showed clear signs of skeletal muscle atrophy and inflammation, but gastrocnemius muscle weight was lower and muscle inflammatory status worse in H-CIA than in CIA. Reduced mitochondrial function was observed only in H-CIA. Prophylactic application of 100 mg/kg lavender oil or linalyl acetate kept IL-6 levels to the normal range and reduced hind paw edema and systolic BP. Linalyl acetate 100 mg/kg was the only treatment that maintained diastolic BP and IGF-1 in their normal ranges and prevented vascular endothelial damage. These treatments also reduced inflammation of the gastrocnemius muscle and inhibited mitochondrial dysfunction while tending to increase muscle mass. Conclusions: Chronic nicotine exposure induces defects that increase the risks of cardiovascular disease and muscle weakness, and application of lavender and linalyl acetate reduced the risks, especially, linalyl acetated alleviated vascular endothelial damage along with maintained IGF-1 level. Current results encourage smokers at high risk for RA to quit smoking, and further suggest that linalyl acetate is a useful agent to prevent cardiovascular and skeletal muscle related comorbidities.

2021 ◽  
Vol 286 ◽  
pp. 02004
Author(s):  
Vanya Gandova ◽  
Stanislava Tasheva ◽  
Vanya Prodanova-Stefanova ◽  
Krasimira Dobreva ◽  
Ivayla Dincheva ◽  
...  

The thermodynamic and physicochemical properties of lavender oil (Lavandula angustifolia Mill.)-ethanol-water system were measured. The chemical composition of solutions of the lavender oil in 70%, 75%, 80%, 85%, 90%, and 95% ethanol was determined using GC/MS analysis. The main compounds in the solutions are oxygenated monoterpenes (β-linalool, terpinen-4-ol, α-terpineol, and linalyl acetate), followed by monoterpene hydrocarbons ((Z)-β-ocimene and (E)-β-ocimene), and sesquiterpene hydrocarbons (β-caryophyllene and (E)-β-farnesene). The ternary phase diagrams were constructed. By multiply linear regression model for surface tension prediction was applied. The thermodynamic and kinetic parameters of lavender oil – ethanol - water system were calculated (energy of Gibb’s, enthalpy, entropy, energy of activation, and coefficient of diffusion).


2014 ◽  
Vol 726 ◽  
pp. 9-15 ◽  
Author(s):  
Li-Hua Yao ◽  
Wei Meng ◽  
Rong-Feng Song ◽  
Qiu-Ping Xiong ◽  
Wei Sun ◽  
...  

2000 ◽  
Vol 78 (4) ◽  
pp. 350-357 ◽  
Author(s):  
Dilson E Rassier ◽  
Brian R MacIntosh

In skeletal muscle, there is a length dependence of staircase potentiation for which the mechanism is unclear. In this study we tested the hypothesis that abolition of this length dependence by caffeine is effected by a mechanism independent of enhanced Ca2+ release. To test this hypothesis we have used caffeine, which abolishes length dependence of potentiation, and dantrolene sodium, which inhibits Ca2+ release. In situ isometric twitch contractions of rat gastrocnemius muscle before and after 20 s of repetitive stimulation at 5 Hz were analyzed at optimal length (Lo), Lo - 10%, and Lo + 10%. Potentiation was observed to be length dependent, with an increase in developed tension (DT) of 78 ± 12, 51 ± 5, and 34 ± 9% (mean ± SEM), at Lo - 10%, Lo, and Lo + 10%, respectively. Caffeine diminished the length dependence of activation and suppressed the length dependence of staircase potentiation, giving increases in DT of 65±13, 53 ± 11, and 45 ± 12% for Lo - 10%, Lo, and Lo + 10%, respectively. Dantrolene administered after caffeine did not reverse this effect. Dantrolene alone depressed the potentiation response, but did not affect the length dependence of staircase potentiation, with increases in DT of 58 ± 17, 26 ± 8, and 18 ± 7%, respectively. This study confirms that there is a length dependence of staircase potentiation in mammalian skeletal muscle which is suppressed by caffeine. Since dantrolene did not alter this suppression of the length dependence of potentiation by caffeine, it is apparently not directly modulated by Ca2+ availability in the myoplasm.


2020 ◽  
Vol 319 (6) ◽  
pp. E1031-E1043
Author(s):  
Xiaodan Lu ◽  
Shengqing Hu ◽  
Yunfei Liao ◽  
Juan Zheng ◽  
Tianshu Zeng ◽  
...  

Caloric restriction (CR) followed by refeeding, a phenomenon known as catch-up growth (CUG), results in excessive lipid deposition and insulin resistance in skeletal muscle, but the underlying mechanisms remain elusive. Recent reports have suggested that vascular endothelial growth factor B (VEGF-B) controls muscle lipid accumulation by regulating endothelial fatty acid transport. Here, we found continuous activation of VEGF-B signaling and increased lipid uptake in skeletal muscle from CR to refeeding, as well as increased lipid deposition and impaired insulin sensitivity after refeeding in the skeletal muscle of CUG rodents. Inhibiting VEGF-B signaling reduced fatty acid uptake in and transport across endothelial cells. Knockdown of Vegfb in the tibialis anterior (TA) muscle of CUG mice significantly attenuated muscle lipid accumulation and ameliorated muscle insulin sensitivity by decreasing lipid uptake. Furthermore, we showed that aberrant histone methylation (H3K9me1) and acetylation (H3K14ac and H3K18ac) at the Vegfb promoter might be the main cause of persistent VEGF-B upregulation in skeletal muscle during CUG. Modifying these aberrant loci using their related enzymes [PHD finger protein 2 (PHF2) or E1A binding protein p300 (p300)] could regulate VEGF-B expression in vitro. Collectively, our findings indicate that VEGF-B can promote transendothelial lipid transport and lead to lipid overaccumulation and insulin resistance in skeletal muscle during CUG, which might be mediated by histone methylation and acetylation.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaoguang Liu ◽  
Xinyu Weng ◽  
Weihua Xiao ◽  
Xin Xu ◽  
Yingjie Chen ◽  
...  

Angiogenesis is an important process under both physiological and pathophysiological conditions. Here we investigated the role and the underlying mechanism of PD-1 in hindlimb ischemia-induced inflammation and angiogenesis in mice. We found that inhibition of PD-1 by genetic PD-1 knockout or pharmacological PD-1 blocking antibodies dramatically attenuated hindlimb blood perfusion, angiogenesis, and exercise capacity in mice after femoral artery ligation. Mechanistically, we found that PD-1 knockout significantly exacerbated ischemia-induced muscle oxidative stress, leukocyte infiltration and IFN-γ production before abnormal angiogenesis in these mice. In addition, we found that the percentages of IFN-γ positive macrophages and CD8 T cells were significantly increased in P-1 knockout mice after hindlimb ischemia. Macrophages were the major leukocyte subset infiltrated in skeletal muscle, which were responsible for the enhanced muscle leukocyte-derived IFN-γ production in PD-1 knockout mice after hindlimb ischemia. Moreover, we demonstrated that IFN-γ significantly attenuated vascular endothelial cell proliferation, tube formation and migration in vitro. IFN-γ also significantly enhanced vascular endothelial cell apoptosis. In addition, the total number of TNF-α positive leukocytes/muscle weight were significantly increased in PD-1-/- mice after hindlimb ischemia. These data indicate that PD-1 exerts an important role in ischemia-induced muscle inflammation and angiogenesis.


2021 ◽  
Vol 10 (16) ◽  
pp. 3507
Author(s):  
Tahmina Nasrin Poly ◽  
Md. Mohaimenul Islam ◽  
Yu-Chuan (Jack) Li ◽  
Ming Chin Lin ◽  
Min-Huei Hsu ◽  
...  

Background and Aims: The coronavirus disease 2019 (COVID-19) increases hyperinflammatory state, leading to acute lung damage, hyperglycemia, vascular endothelial damage, and a higher mortality rate. Metformin is a first-line treatment for type 2 diabetes and is known to have anti-inflammatory and immunosuppressive effects. Previous studies have shown that metformin use is associated with decreased risk of mortality among patients with COVID-19; however, the results are still inconclusive. This study investigated the association between metformin and the risk of mortality among diabetes patients with COVID-19. Methods: Data were collected from online databases such as PubMed, EMBASE, Scopus, and Web of Science, and reference from the most relevant articles. The search and collection of relevant articles was carried out between 1 February 2020, and 20 June 2021. Two independent reviewers extracted information from selected studies. The random-effects model was used to estimate risk ratios (RRs), with a 95% confidence interval. Results: A total of 16 studies met all inclusion criteria. Diabetes patients given metformin had a significantly reduced risk of mortality ((RR 0.65; 95% CI: 0.54–0.80, p < 0.001, heterogeneity I2 = 75.88, Q = 62.20, and τ2 = 0.06, p < 0.001)) compared with those who were not given metformin. Subgroup analyses showed that the beneficial effect of metformin was higher in the patients from North America (RR 0.43; 95% CI: 0.26–0.72, p = 0.001, heterogeneity I2 = 85.57, Q = 34.65, τ2 = 0.31) than in patients from Europe (RR 0.67; 95% CI: 0.47–0.94, p = 0.02, heterogeneity I2 = 82.69, Q = 23.11, τ2 = 0.10) and Asia (RR 0.90; 95% CI: 0.43–1.86, p = 0.78, heterogeneity I2 = 64.12, Q = 11.15, τ2 = 0.40). Conclusion: This meta-analysis shows evidence that supports the theory that the use of metformin is associated with a decreased risk of mortality among diabetes patients with COVID-19. Randomized control trials with a higher number of participants are warranted to assess the effectiveness of metformin for reducing the mortality of COVID-19 patients.


2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Elisa Benetti ◽  
Raffaella Mastrocola ◽  
Mara Rogazzo ◽  
Fausto Chiazza ◽  
Manuela Aragno ◽  
...  

Peroxisome Proliferator Activated Receptor (PPAR)-δagonists may serve for treating metabolic diseases. However, the effects of PPAR-δagonism within the skeletal muscle, which plays a key role in whole-body glucose metabolism, remain unclear. This study aimed to investigate the signaling pathways activated in the gastrocnemius muscle by chronic administration of the selective PPAR-δagonist, GW0742 (1 mg/kg/day for 16 weeks), in male C57Bl6/J mice treated for 30 weeks with high-fructose corn syrup (HFCS), the major sweetener in foods and soft-drinks (15% wt/vol in drinking water). Mice fed with the HFCS diet exhibited hyperlipidemia, hyperinsulinemia, hyperleptinemia, and hypoadiponectinemia. In the gastrocnemius muscle, HFCS impaired insulin and AMP-activated protein kinase signaling pathways and reduced GLUT-4 and GLUT-5 expression and membrane translocation. GW0742 administration induced PPAR-δupregulation and improvement in glucose and lipid metabolism. Diet-induced activation of nuclear factor-κB and expression of inducible-nitric-oxide-synthase and intercellular-adhesion-molecule-1 were attenuated by drug treatment. These effects were accompanied by reduction in the serum concentration of interleukin-6 and increase in muscular expression of fibroblast growth factor-21. Overall, here we show that PPAR-δactivation protects the skeletal muscle against the metabolic abnormalities caused by chronic HFCS exposure by affecting multiple levels of the insulin and inflammatory cascades.


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