Lagerstroemia ovalifolia Exerts Anti- Inflammatory Effects in Mice of LPSInduced ALI via Downregulating of MAPK and NF-κB Activation

Abstract

Lagerstroemia ovalifoliaTeijsm. & Binn. (LO) (crape myrtle) has reportedly been used as traditional herbal medicine (THM) in Java, Indonesia. Our previous study revealed that the LO leaf extract (LOLE) exerted anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Based on this finding, the current study aimed to evaluate the protective effects of LOLE in a mouse model of LPS-induced acute lung injury (ALI). The results showed that treatment with LPS enhanced the inflammatory cell influx into the lungs and increased the number of macrophages and the secretion of the inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of mice. However, these effects were notably abrogated with LOLE pretreatment. Furthermore, the increase of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and monocyte chemoattractant protein-1 (MCP-1) expression in the lung tissues of mice with ALI was also reversed by LOLE. In addition, LOLE significantly suppressed the LPS-induced activation of the MAPK/NF-κB signaling pathway and led to heme oxygenase-1 (HO-1) induction in the lungs. Additionally, in vitro experiments showed that LOLE enhanced the expression of HO-1 in RAW264.7 macrophages. The aforementioned findings collectively indicate that LOLE exerts an ameliorative effect on inflammatory response in the airway of ALI mice.

Protective Effect of Paulownia tomentosa Fruits in an Experimental Animal Model of Acute Lung Injury

“…As mentioned earlier, the expression of inflammatory cytokines, chemokines and mediators is associated with MAPK and NF-κB activation in ALI development [2,23,24]. Therefore, targeting MAPK and NF-κB signaling pathways has been suggested as a potential strategy for the prevention or treatment of ALI [6,13,18]. In the present study, PTF reduced TNF-α, IL-6 and MCP-1 secretion, as well as iNOS and COX-2 expression, in ALI mice.…”

“…Male C57BL/6 mice (n = 30; age, 6 weeks old; body weight, 18 ± 1 g) were purchased from Koatech Co., Ltd. All experimental procedures were approved by the Institutional Animal Care and Use Committee of the KRIBB (KRIBB-AEC-21111). To induce ALI, mice were administered LPS intranasally, as previously described [6]. The experimental groups used for the in vivo study were divided into the following five groups: Normal control (NC group), ALI (LPS only group), LPS + dexamethasone (DEX; LPS + 1 mg/kg DEX group), LPS + PTF 10 (LPS + 10 mg/kg PTF group) and LPS + PTF 20 (LPS + 20 mg/kg PTF group).…”

“…It has been reported that the upregulation of tumor necrosis factor-α (TNF-α) and interleukine-6 (IL-6) promotes inflammatory response in the airways during ALI development [3−5]. Macrophage-released monocyte chemoattractant protein 1 (MCP-1) elevates airway inflammation, leading to inflammatory cell influx [5,6]. In ALI pathogenesis, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) cause peroxynitrite generation and pain sensitization, respectively [7,8].…”

Advances in the use of exosomes for the treatment of ALI/ARDS

“…The mitogen-activated protein kinase (MAPK) signaling pathway is important in eukaryotes and can be activated by a variety of extracellular and intracellular signals or stimuli such as cytokines, hormones, and various stressors ( 110 ). As the MAPK signaling pathway plays a key role in cell growth, migration, proliferation, differentiation, and apoptosis, this pathway is involved in the pathogenesis of human diseases including ALI/ARDS ( 111 , 112 ).…”