Anti-Inflammatory Effects of Apigenin in Lipopolysaccharide-Induced Inflammatory in Acute Lung Injury by Suppressing COX-2 and NF-kB Pathway

Abstract

This study aims to evaluate the possible mechanisms responsible for the anti-inflammatory effects of apigenin lipopolysaccharide (LPS)-induced inflammatory in acute lung injury. In this study, the anti-inflammatory effects of apigenin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the possible mechanisms involved in this protection were investigated. Pretreatment with apigenin prior to the administration of intratracheal LPS significantly induced a decrease in lung wet weight/dry weight ratio in total leukocyte number and neutrophil percent in the bronchoalveolar lavage fluid (BALF) and in IL-6 and IL-1β, the tumor neurosis factor-α (TNF-α) in the BALF. These results showed that anti-inflammatory effects of apigenin against the LPS-induced ALI may be due to its ability of primary inhibition of cyclooxygenase-2 (COX-2) gene expression and nuclear factor kB (NF-kB) gene expression of lung. The results presented here suggest that the protective mechanism of apigenin may be attributed partly to decreased production of proinflammatory cytokines through the inhibition of COX-2 and NF-kB activation. The results support that use of apigenin is beneficial in the treatment of ALI.

Plant polyphenols as inhibitors of NF-κB induced cytokine production—a potential anti-inflammatory treatment for Alzheimer's disease?

“…Among the polyphenols that have been shown to modulate pro-inflammatory gene expression are curcumin (Jobin et al, 1999), apigenin (Wang et al, 2014), resveratrol (Kundu et al, 2006), quercetin (Endale et al, 2013), silymarin (Saliou et al, 1998) cinnamaldehyde (Reddy et al, 2004), pathenolode (Saadane et al, 2007), ergolide (Chun et al, 2007), 2β,5-epoxy-5,10-dihydroxy-6α-angeloyloxy-9β-isobutyloxy-germacran-8α,12-olide (Lee et al, 2011), andalusol (Heras et al, 1999), ent-kaur-16-ene-19-oic acid (Wu et al, 2013), kamebanin (Hwang et al, 2001), kamebacetal A (Hwang et al, 2001), kamebakaurin (Hwang et al, 2001), excisanin A (Hwang et al, 2001), hypoestoxide(Ojo-Amaize et al, 2001), helenalin (Lyss et al, 1997), pristimerin (Tiedemann et al, 2009), epigallocatechin gallate (Kim et al, 2010), avicin (Haridas et al, 2001), capsaicin (Singh et al, 1996), and oleandrin (Sreenivasan et al, 2003), just to name a few. In this opinion paper, we will focus on curcumin as the prime example as the manuscript format does not allow to elaborate on the specific targets of each of the compounds in the NF-κB pathway.…”

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

“…These acute inflammatory responses can be summarized as inflammatory cell accumulation, leakage of protein into the alveolar space, interstitial edema and disruption of epithelial integrity [4]. NF-κB is required for maximal transcription of many cytokines, including pro-inflammatory mediator tumor necrosis factor (TNF)-α, and interleukin (IL)-1β.…”

Effect and mechanism of evodiamine against ethanol-induced gastric ulcer in mice by suppressing Rho/NF-кB pathway

“…One of the most widely recognized intracellular signaling pathway in inflammatory responses is the nuclear factor kappa B (NF-κB) signaling pathway [7]. Expressed in almost all cells, NF-κB participate in the regulation of various genes involved in immune response and acute phase inflammatory reaction [8].…”