Scutellaria baicalensis Ameliorates Acute Lung Injury by Suppressing Inflammation In Vitro and In Vivo

Chen, Jian-Jung; Huang, Chung-Chun; Chang, Heng-Yuan; Li, Peiying; Liang, Yu-Chia; Deng, Jeng-Shyan; Huang, Shyh-Shyun; Huang, Guan‐Jhong

doi:10.1142/s0192415x17500100

Cited by 34 publications

(25 citation statements)

References 27 publications

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“…IL-6 is increased in the BALF of patients and higher levels increase mortality, which is identified as one of the biomarkers in monitoring ALI [48]. In addition, MPO activity is a sensitive and specific marker for ALI that is used to assess the quantification of neutrophil accumulation in tissues [49]. Notably, miR-27a has been reported to be associated with inflammatory mediator production [26], which promoted us to verify whether miR- Figure 6.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inﬂammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway

et al. 2018

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Acute lung injury (ALI) is a critical clinical condition with a high mortality rate, characterized with excessive uncontrolled inflammation and apoptosis. Recently, microRNAs (miRNAs) have been found to play crucial roles in the amelioration of various inflammation-induced diseases, including ALI. However, it remains unknown the biological function and regulatory mechanisms of miRNAs in the regulation of inﬂammation and apoptosis in ALI. The aim of this study is to identify and evaluate the potential role of miRNAs in ALI and reveal the underlying molecular mechanisms of their effects. Here, we analyzed microRNA expression profiles in lung tissues from LPS-challenged mice using miRNA microarray. Because microRNA-27a (miR-27a) was one of the miRNAs being most significantly downregulated, which has an important role in regulation of inflammation, we investigated its function. Overexpression of miR-27a by agomir-27a improved lung injury, as evidenced by the reduced histopathological changes, lung wet/dry (W/D) ratio, lung microvascular permeability and apoptosis in the lung tissues, as well as ameliorative survival of ALI mice. This was accompanied by the alleviating of inflammation, such as the reduced total BALF cell and neutrophil counts, decreased levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-6) interleukin-1β (IL-1β) and myeloperoxidase (MPO) activity in BAL fluid. Toll-like receptor 4 (TLR4), an important regulator of the nuclear factor kappa-B (NF-κB) signaling pathway, was identified as a novel target of miR-27a in RAW264.7 cells. Furthermore, our results showed that LPS stimulation increased the expression of MyD88 and NF-κB p65 (p-p65), but inhibited the expression of inhibitor of nuclear factor-κB-α (IκB-α), suggesting the activation of NF-κB signaling pathway. Further investigations revealed that agomir-miR-27a reversed the promoting effect of LPS on NF-κB signaling pathway. The results here suggested that miR-27a alleviates LPS-induced ALI in mice via reducing inﬂammation and apoptosis through blocking TLR4/MyD88/NF-κB activation.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inﬂammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway

et al. 2018

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“…Scutellaria baicalensis is a perennial herb of the genus Scutellaria in Labiatae and it is one of the most popular TCMs used for inflammation, cancer, and bacterial and viral infections in China (Chen et al, ). Baicalin is a flavonoid taken out from the dried root of Scutellaria baicalensis .…”

Section: Introductionmentioning

confidence: 99%

Retracted: Baicalin relieves lipopolysaccharide‐evoked inflammatory injury through regulation of miR‐21 in H9c2 cells

Liu

Wang

Zhao

2020

Phytotherapy Research

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Myocarditis is a common heart disease which lacks effective treatment till now.Baicalin possesses plenty of activities, including anti-inflammation. In this investigation, we attempted to investigate the influences of Baicalin on Lipopolysaccharide (LPS)-evoked H9c2 cells.Cells viability, apoptosis, and expressions of apoptosisassociated proteins were, respectively, measured utilizing CCK-8 assay, flow cytometry and western blot. The levels of IL-6 and TNF-α were detected through enzyme-linked immunosorbent assay, western blot and qRT-PCR. miR-21 expression was detected through qRT-PCR and was silenced using cell transfection. The expressions of NF-κB and PDCD4/JNK pathways related proteins were measured through western blot. We found that LPS stimulation induced cell apoptosis and upregulation of IL-6 and TNF-α. Baicalin treatment effectively suppressed LPS-induced inflammation and apoptosis. The NF-κB and PDCD4/JNK pathways were blocked by Baicalin. Additionally, the enhanced expression of miR-21 triggered by LPS was further elevated by Baicalin. Further study revealed that the inhibiting effects of Baicalin on LPS-evoked injury were largely attenuated by knockdown of miR-21. Moreover, the associated NF-κB and JNK pathways, which were suppressed by Baicalin treatment, were then activated by knockdown of miR-21. Our present study revealed that Baicalin alleviated LPS-evoked inflammatory injury via suppressing the NF-κB and PDCD4/JNK pathways through regulating miR-21 expression. K E Y W O R D S apoptosis, Baicalin, inflammatory injury, MiR-21, myocarditis

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“…MPO activity is a sensitive and specific marker for acute lung injury that is used to assess the quantification of neutrophil accumulation in tissues [ 24 ]. The present study was carried out to evaluate whether the AVA treatment significantly reduced the number of total cells in BALF and the MPO activity in lung tissues compared with the LPS group.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of Velvet Antler (Cervus elaphus) against Lipopolysaccharide‐Induced Acute Lung Injury in Mice by Inhibiting MAPK/NF‐κB Activation and Inducing AMPK/Nrf2 Pathways

Chang

Lin

Deng

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Velvet antler (Cervus elaphus) is a typical traditional animal medicine. It is considered to have various pharmacological effects including stimulation of the immune system, increase in the physical strength, and enhancement of sexual function. This paper aims to investigate the aqueous extract of velvet antler (AVA) in the mouse models of LPS-induced ALI. Inhibition of NO, TNF-α, IL-1β, IL-6, and IL-10 productions contributes to the attenuation of LPS-induced lung inflammation by AVA. A 5-day pretreatment of AVA prevented histological alterations and enhanced antioxidant enzyme activity in lung tissues. AVA significantly reduced the material (total number of cells and proteins) in the BALF. Western blot analysis revealed that the expression of iNOS and COX-2 and phosphorylation of IκB-α and MAPKs proteins are blocked in LPS-stimulated macrophages as well as LPS-induced lung injury in mice. Consistent with this concept, the phosphorylation of CaMKKβ, LKB1, AMPK, Nrf2, and HO-1 was activated after AVA treatment. The results from this study indicate AVA has anti-inflammatory effects in vivo and AVA is a potential model for the development of health food. In addition, its pathways may be at least partially associated with inhibiting MAPK/NF-κB activation and upregulating AMPK/Nrf2 pathways and the regulation of antioxidant enzyme activity.

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Scutellaria baicalensis Ameliorates Acute Lung Injury by Suppressing Inflammation In Vitro and In Vivo

Cited by 34 publications

References 27 publications

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inﬂammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inﬂammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway

Retracted: Baicalin relieves lipopolysaccharide‐evoked inflammatory injury through regulation of miR‐21 in H9c2 cells

Preventive Effects of Velvet Antler (Cervus elaphus) against Lipopolysaccharide‐Induced Acute Lung Injury in Mice by Inhibiting MAPK/NF‐κB Activation and Inducing AMPK/Nrf2 Pathways

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