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Acute lung injury (ALI) is a life-threatening clinical syndrome with high morbidity and mortality. The main pathological features of ALI are increased alveolar-capillary membrane permeability, edema, uncontrolled migration of neutrophils to the lungs, and diffuse alveolar damage, resulting in acute hypoxemic respiratory failure. Glucocorticoids, aspirin, and other anti-inflammatory drugs are commonly used to treat ALI. Respiratory supports, such as a ventilator, are used to alleviate hypoxemia. Many treatment methods are available, but they cannot significantly ameliorate the quality of life of patients with ALI and reduce mortality rates. Herbal active ingredients, such as flavonoids, terpenoids, saponins, alkaloids, and quinonoids, exhibit advantages for ALI prevention and treatment, but the underlying mechanism needs further study. This paper summarizes the role of herbal active ingredients in anti-ALI therapy and progresses in the understanding of their mechanisms. The work also provides some references and insights for the discovery and development of novel drugs for ALI prevention and treatment.

Salidroside (SDS) has been reported to have anti-inflammatory properties. The objective of this study was to investigate the protective effect of SDS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. BALB/c mice were pretreated with SDS 1 hour before intranasal instillation of LPS. Seven hours after LPS administration, the myeloperoxidase in histology of lungs, lung wet/dry ratio, and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The levels of pro-inflammatory cytokines, tumor necrosis factor α (TNF-α), interleukin-1β (IL 1β), and IL-6 in the BALF were measured by enzyme-linked immunosorbent assay. The expression of Toll-like receptor 4 (TLR4), inhibitor of nuclear factor-kappa B (IκB-α), and nuclear factor-kappa B (NF-κB) p65 was detected by Western blot. The SDS reduced the inflammatory cells in BALF, decreased the wet/dry ratio of lungs, attenuated the LPS-induced histological alterations in the lung, and inhibited the production of TNF-α, IL-1β, and IL-6. Western blot showed that SDS efficiently inhibited the phosphorylation of IκB-α, p65 NF-κB, and the expression of TLR4. These data show that the anti-inflammatory effects of SDS (at least 20 mg/kg) against LPS-induced ALI due to its ability to inhibit TLR4 mediated the NF-κB signaling pathways. The SDS may represent a novel strategy for treating LPS-induced ALI.

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The objective of this work was to explore the hypothesis that Lycium barbarum (LB) may be protective against doxorubicin (DOX)-induced cardiotoxicity through antioxidant-mediated mechanisms. Male SD rats were treated with distilled water or a water extract of LB (25 mg/kg, p.o.) daily and saline or DOX (5 mg/kg, i.v.) weekly for 3 weeks. Mortality, general condition and body weight were observed during the experiment. DOX-induced cardiotoxicity was assessed by electrocardiograph, heart antioxidant activity, serum levels of creatine kinase (CK) and aspartate aminotransferase (AST) and histopathological change. The DOX group showed higher mortality (38%) and worse physical characterization. Moreover, DOX caused myocardial injury manifested by arrhythmias and conduction abnormalities in ECG (increased QT and ST intervals and ST elevation), a decrease of heart antioxidant activity, an increase of serum CK and AST, as well as myocardial lesions. Pretreatment with LB significantly prevented the loss of myofibrils and improved the heart function of the DOX-treated rats as evidenced from lower mortality (13%), normalization of antioxidative activity and serum AST and CK, as well as improving arrhythmias and conduction abnormalities. These results suggested that LB elicited a typical cardioprotective effect on DOX-related oxidative stress. Furthermore, in vitro cytotoxic study showed the antitumor activity of DOX was not compromised by LB. It is possible that LB could be used as a useful adjunct in combination with DOX chemotherapy.