Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Abstract

The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC‐5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK‐8, FITC‐PI double staining, Western blot, qRT‐PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual‐luciferase assay was used to detect the targeting link between miR‐103 and lipoprotein receptor‐related protein 1 (LRP1). LPS induced apoptosis and the release of MCP‐1, IL‐6 and TNF‐α in MRC‐5 cells. Pre‐treating MRC‐5 cells with gastrodin attenuated LPS‐induced cell damage. Meanwhile, p38/JNK and NF‐κB pathways induced by LPS were repressed by gastrodin. miR‐103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR‐103 silencing. And LRP1 was a target of miR‐103 and negatively regulated by miR‐103. The in vitro data illustrated the protective function of gastrodin in LPS‐injured MRC‐5 cells. Gastrodin exerted its function possibly by up‐regulating miR‐103 and modulating p38/JNK and NF‐κB pathways.

Diagnostic Value of miR-103 in Patients with Sepsis and Noninfectious SIRS and Its Regulatory Role in LPS-Induced Inflammatory Response by Targeting TLR4

“…Previous studies have showed that miR-103 plays an important regulatory role in inflammatory responses, such as the inhibiting effect of miR-103 on inflammation in obesity and metabolic syndrome-related disorders [29], chronic obstructive pulmonary disease [30], and Alzheimer's disease [15]. In the present study, the serum miR-103 was found to be negatively correlated with inflammatory cytokine levels in sepsis patients.…”

The up-regulation of miR-21 by gastrodin to promote the angiogenesis ability of human umbilical vein endothelial cells by activating the signaling pathway of PI3K/Akt

“…Liu et al found that gastrodin antagonized the up-regulation of stress signals from the endoplasmic reticulum by activating the Nrf2 pathway, including the expression of GRP78, CHOP, and phosphorylated eIF2α, reducing osteoporosis in rats caused by glucocorticoids [ 20 ]. Zhuo et al found that adding gastrodin to the cell model MRC-5 of chronic obstructive pulmonary disease can suppress the LPS-induced activation of p38/JNK and NF-κB pathways by down-regulating the miR-103 expression [ 21 ]. It can be seen that gastrodin plays a positive effect in the disease treating, and exert a certain protective effect on the body.…”

Gastrodin attenuates lipopolysaccharide‑induced inflammation and oxidative stress, and promotes the osteogenic differentiation of human periodontal ligament stem cells through enhancing sirtuin3 expression

“…For example, GAS was demonstrated to ameliorate cerebral ischemic injury by inhibiting inflammation and apoptosis in animal models (9)(10)(11)(12). In addition, previous studies suggested that GAS may attenuate lipopolysaccharide (LPS)-induced inflammation and apoptosis in lung cells both in vitro and in vivo (13,14). In particular, the protective effect of GAS on bone-related diseases has also been reported.…”