Salidroside Attenuates Airway Inflammation and Remodeling via the miR-323-3p/SOCS5 Axis in Asthmatic Mice

Ming, Xi; Yu, Xingzhu; Li, Jijun; Wang, Junyu; Zheng, Jialin; Xiong, Lei

doi:10.1159/000520444

Cited by 9 publications

(7 citation statements)

References 37 publications

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“… 39 Furthermore, salidroside has been shown to alleviate airway inflammation and remodeling in asthmatic mice by suppressing the expression of the miR-323-3p in the cytokine signaling 5 (SOCS5). 40 In this study, we showed that salidroside inhibited miRNA-199a-5p, increased the TNFAIP8L2, decreased the HMGB1/TLR4/NF-κB signaling pathway, decreased the secretion of inflammatory cytokine molecules in the MLE-12 cells, and assuaged the endotoxin-induced acute lung injuries.…”

Section: Discussionmentioning

confidence: 65%

The protective mechanism of salidroside modulating miR-199a-5p/TNFAIP8L2 on lipopolysaccharide-induced MLE-12 cells

Tan

Zou

Zhang

et al. 2022

Int J Immunopathol Pharmacol

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Objectives Salidroside is used for treating inflammation-based diseases; however, its molecular mechanism is unclear. In this study, we determined the protective role of salidroside on the endotoxin-induced damage caused to the mouse alveolar epithelial type II (MLE-12) cells and its underlying mechanism. Methods An in vitro model for acute lung injury was constructed by inducing the MLE-12 cells using lipopolysaccharide (lipopolysaccharides, 1 mg/L). Then, The MTT assay was conducted to assess the survival rate of the MLE-12 cells in the different groups. After the treatment, apoptosis of MLE-12 cells was determined, and the mRNA and protein expression of miR-199a-5p, HMGB1, NF-kB65, TNFAIP8L2, p-IkB-α, and TLR4 was estimated by Western Blotting and RT-PCR. ELISA was also used to measure the concentration of inflammatory cytokine molecules IL-1β, IL-6, TNF-α, and IL-18 in the cell-free supernatant. Lastly, cell morphology was examined using the AO/EB technique. Results We showed that salidroside reduced the protein and gene expression of HMGB1, NF-kB65, miR-199a-5p, p-IkB-α, and TLR4, whereas it increased the gene and protein expression of TNFAIP8L2. Furthermore, it decreased the concentrations of cytokine molecules like IL-1β, IL-6, TNF-α, and IL-18 in the cell-free supernatant. MLE-12 also showed a lower apoptosis rate, higher survival rate, and better cell morphology. Conclusion Salidroside significantly inhibited the LPS-induced MLE-12 cell damage. Our results suggest that this could be by reducing miR-199a-5p and enhancing TNFAIP8L2 expression.

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Section: Discussionmentioning

confidence: 65%

The protective mechanism of salidroside modulating miR-199a-5p/TNFAIP8L2 on lipopolysaccharide-induced MLE-12 cells

Tan

Zou

Zhang

et al. 2022

Int J Immunopathol Pharmacol

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“…Salidroside, which is extracted from the root of Rhodiola rosea L, plays a critical role in multiple processes, like anti‐oxidation, anti‐aging, cancer‐related therapy, and especially in anti‐inflammation (Fan, Su, et al, 2022; Fan, Xu, et al, 2022; Jin et al, 2016; Ma et al, 2021; Wang et al, 2022). Researchers found that salidroside could ameliorate ovalbumin‐induced airway inflammation and hyperresponsiveness in asthma mice and inhibit the microglial inflammation induced by hypoxia (Fan, Su, et al, 2022; Fan, Xu, et al, 2022; Luan et al, 2022; Ming et al, 2022). Besides, it was also reported that salidroside could alleviate furan‐induced liver inflammation and improve the P4HB‐mediated inflammation of skin (Ding et al, 2020; Yuan et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Salidroside ameliorated the pulmonary inflammation induced by cigarette smoke via mitigating M1 macrophage polarization by JNK/c‐Jun

Feng

Zhang

Yin

et al. 2023

Phytotherapy Research

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Pulmonary inflammation induced by cigarette smoke (CS) promoted the development of chronic obstructive pulmonary disease (COPD), and macrophage polarization caused by CS modulated inflammatory response. Previous studies indicated that salidroside exerted therapeutic effects in COPD, but the anti‐inflammatory mechanisms were not clear. This study aimed to explore the effects and mechanisms of salidroside on macrophage polarization induced by CS. Wistar rats received passively CS exposure and were treated intraperitoneally with salidroside at a low, medium or high dose. Lung tissues were stained with hematoxylin–eosin. Emphysema and inflammatory scores were evaluated by histomorphology. Lung function, cytokines, and cell differential counts in BALF were detected. The macrophage polarization was determined by immunohistochemistry in lung tissues. Alveolar macrophages (AMs) were isolated and treated with cigarette smoke extract (CSE), salidroside or inhibitors of relative pathways. The polarization status was determined by qPCR, and the protein level was detected by Western blotting. CS exposure induced emphysema and lung function deterioration. The inflammatory scores, cytokines level and neutrophils counts were elevated after CS exposure. Salidroside treatment partly ameliorated above abnormal. CS exposure activated M1 and M2 polarization of AMs in vivo and in vitro, and salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c‐Jun in AMs and the M1 polarization of AMs was inhibited by the inhibitors of JNK and AP‐1. Salidroside treatment deactivated the JNK/c‐Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via inhibiting JNK/c‐Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs induced by CS, and the process might be mediated by the deactivation of JNK/c‐Jun.

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“…SOCS family proteins are a class of negative regulators of JAK2-STAT3 signaling pathway, consisting of SOCS1-7, both containing Src-homology domian and a conserved C-termial domain [ 46 ]. Among them, SOCS5 is expressed in a variety of adult tissues, playing anti-inflammatory, anti-tumor, anti-oxidative stress and other functions [ 16 , 47 , 48 ]. Xi et al uncovered that salidroside could promote SOCS5 transcription to reduce airway inflammation and airway remodeling in asthmatic mice [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

“…Among them, SOCS5 is expressed in a variety of adult tissues, playing anti-inflammatory, anti-tumor, anti-oxidative stress and other functions [ 16 , 47 , 48 ]. Xi et al uncovered that salidroside could promote SOCS5 transcription to reduce airway inflammation and airway remodeling in asthmatic mice [ 48 ]. Tsai et al also proved that SOCS5 was highly expressed in high glucose-induced renal mesangial cells, which led to the inactivation of JAK2/STAT3 pathway [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Sequential inspiratory muscle exercise-noninvasive positive pressure ventilation alleviates oxidative stress in COPD by mediating SOCS5/JAK2/STAT3 pathway

Lei,

He,

et al. 2023

BMC Pulm Med

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Background Pulmonary rehabilitation training is of great significance for the prognosis of chronic obstructive pulmonary disease (COPD) patients. The purpose of this study was to investigate the therapeutic effect and pathway of a new sequential noninvasive positive pressure ventilation (NIPPV) + inspiratory muscle training (IMT) therapy. Methods A total of 100 COPD patients were enrolled and randomly divided into oxygen therapy (OT), NIPPV, IMT and sequential (NIPPV + IMT) group. Lung function, exercise endurance, quality of life, and dyspnea symptoms were examined and recorded. Then, reactive oxygen species (ROS), malonaldehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels were detected by enzyme-linked immunoassay, and suppressor of cytokine signaling 5 (SOCS5)/janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway expression changes were detected by quantitative real time-polymerase chain reaction (qRT-PCR) and western blot. A mouse model of COPD was then established to further verify the effects of SOCS5/JAK2/STAT3 pathways on lung function and oxidative stress. Results After 8 weeks of treatment, NIPPV, IMT or sequential (NIPPV + IMT) significantly improved exercise endurance, quality of life and dyspnea, reduced oxidative stress, promoted SOCS5 expression and inhibited the activation of JAK2/STAT3 pathway, and no significant effect was observed on lung function of COPD patients. Notably, sequential (NIPPV + IMT) showed better therapeutic outcomes than either IMT or NIPPV alone. Moreover, results at the animal level showed that overexpression of SOCS5 significantly reduced pulmonary inflammatory infiltration, pathological changes and oxidative stress levels in COPD mice, enhanced lung function, and inhibited the activation of JAK2/STAT3 pathway. Conclusion Our results elucidated that sequential (NIPPV + IMT) significantly relieved COPD development by regulating SOCS5/JAK2/STAT3 signaling-mediated oxidative stress.

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Salidroside Attenuates Airway Inflammation and Remodeling via the miR-323-3p/SOCS5 Axis in Asthmatic Mice

Cited by 9 publications

References 37 publications

The protective mechanism of salidroside modulating miR-199a-5p/TNFAIP8L2 on lipopolysaccharide-induced MLE-12 cells

The protective mechanism of salidroside modulating miR-199a-5p/TNFAIP8L2 on lipopolysaccharide-induced MLE-12 cells

Salidroside ameliorated the pulmonary inflammation induced by cigarette smoke via mitigating M1 macrophage polarization by JNK/c‐Jun

Sequential inspiratory muscle exercise-noninvasive positive pressure ventilation alleviates oxidative stress in COPD by mediating SOCS5/JAK2/STAT3 pathway

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