Tamarix chinensis Lour. (T. chinensis) is a traditional herb with functions for releasing the exterior to promote the eruption of rashes, among other ailments. However, these function-related pharmacological effects, such as anti-complement, anti-oxidative, and anti-inflammatory, remain unclear. This study aims to reveal the aforementioned effects and the molecular mechanisms of the ethanol extract of T. chinensis (TCE). Our results demonstrated that TCE inhibited classical- and lectin-mediated complement activation, reduced intracellular ROS via NADPH oxidase inhibition, and directly scavenged DPPH radicals and superoxide anions. By using lipopolysaccharide (LPS)-stimulated macrophages, along with LPS-induced acute lung injury (ALI) and endotoxemia mice, the anti-inflammatory activity and the underlying molecular mechanisms of TCE were deeply investigated. In LPS-activated macrophages, it suppressed iNOS, CCL2, IL-6 and IL-1β transcriptionally and translationally. Mechanistically, TCE inhibited NF-κB signaling by blocking IκBα phosphorylation and p65 nuclear translocation, as well as suppresses AP-1 signaling by reducing ERK and JNK phosphorylation. In vivo, TCE lowered serum multiple pro-inflammatory cytokines of endotoxemic mice and alleviated lung injury of ALI mice. Collectively, our results demonstrated that TCE possesses anti-complement and anti-oxidative activities and exerts anti-inflammatory effects through inhibiting NF-κB and AP-1 signaling. These findings provide scientific evidence for supporting the traditional use of T. chinensis.
Wang et al. (Sat,) studied this question.
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