RESUMEN
In China, baicalin is the main active component of Scutellaria baicalensis, which has been used in the treatment of inflammation-related diseases, such as inflammation-induced acute lung injury. However, its specific mechanism remains unclear. This study examined the protective effect of baicalin on LPS-induced inflammation injury of alveolar epithelial cell line A549 and explored its protective mechanism. Compared with the LPS-induced group, the proliferation inhibition rates of alveolar type II epithelial cell line A549 intervened by different concentrations of baicalin decreased significantly, as did the levels of inflammatory factors IL-6, IL-1ß, prostaglandin 2 and TNF-α in the supernatant. The expression levels of inflammatory proteins inducible NO synthase (iNOS), NF-κB65, phosphorylated ERK (p-ERK1/2), and phosphorylated c-Jun N-terminal kinase (p-JNK1) significantly decreased, as did the protein expression of follistatin-like protein 1 (FSTL1). In contrast, expression of miR-200b-3p significantly increased in a dose-dependent manner. These results suggested that baicalin could significantly inhibit the expression of inflammation-related proteins and improve LPS-induced inflammatory injury in alveolar type II epithelial cells. The mechanism may be related to the inhibition of ERK/JNK inflammatory pathway activation by increasing the expression of miR-200b-3p. Thus, FSTL1 is the regulatory target of miR-200b-3p.
Asunto(s)
Células Epiteliales/efectos de los fármacos , Células Epiteliales/patología , Flavonoides/uso terapéutico , Proteínas Relacionadas con la Folistatina/efectos de los fármacos , Lipopolisacáridos , MicroARNs/biosíntesis , Alveolos Pulmonares/lesiones , Transducción de Señal/efectos de los fármacos , Células A549 , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Humanos , Inflamación/inducido químicamente , Inflamación/patología , Mediadores de Inflamación/metabolismo , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , MicroARNs/efectos de los fármacos , MicroARNs/genética , Alveolos Pulmonares/efectos de los fármacos , Alveolos Pulmonares/patologíaRESUMEN
Adipokines are mediators of body composition and are involved in obesity-related complications such as cardiovascular disease. Omega-3 supplementation has not been studied in the setting of body composition and follistatin-like 1 (FSTL1) levels in patients with coronary artery disease (CAD). This study aimed to investigate the effect of omega-3 polyunsaturated fatty acid (ω-3 PUFA) supplementation on body composition indices and serum levels of FSTL1 in CAD patients. A total of 42 male (aged 45-65 years) subjects with angiographically confirmed CAD were included in this randomized, double-blind, placebo-controlled trial study. The subjects were randomly divided into omega-3 and placebo groups. During the 8-week intervention, the omega-3 group received 1,200 mg of omega-3 daily, while the placebo group received paraffin. Before and after the study, anthropometric measurements and body composition components were taken; serum FSTL1 levels were assessed by an enzyme-linked immunosorbent assay (ELISA) kit. In the omega-3 group, a significant 27.6% increase in serum FSTL1 was seen after 8 weeks of intervention ( p = .001), but no significant difference in posttreatment levels of FSTL1 was observed between the two groups ( p > .05). At the end of the study, a significant decrease in low-density lipoprotein cholesterol (LDL-C; 94.29 ± 22.04 vs. 112.24 ± 24.5; p = .01) and high-sensitivity C-reactive protein (hs-CRP; 1.92 ± 0.79 vs. 3.19 ± 2.51; p = .03) concentration was detected between the two groups. Changes in fasting blood sugar, fasting insulin, body composition, and anthropometric parameters were not significant within and between the groups. Oral omega-3 might increase FSTL1 and decrease LDL-C and hs-CRP concentrations in CAD patients. However, omega-3 supplementation did not have any effect on FSTL1 levels between the groups.