Anti-inflammatory effect and component analysis of Chaihu Qingwen granules.

ETHNOPHARMACOLOGICAL RELEVANCE: As prevalent acute respiratory condition in clinical practice, acute lung injury has a quick start and severe symptoms which can harm patients physically. Chaihu Qingwen granules (CHQW) is a classic formula for the treatment of respiratory diseases. Clinical observation shows that CHQW has good efficacy in treating colds, coughs, and fevers. AIM OF THE STUDY: The aim of this study was to investigate the anti-inflammatory effect of CHQW on lipopolysaccharide (LPS)-induced acute lung injury (ALI) model in rats and to explore its potential mechanism, as well as to clarify its substance composition. MATERIALS AND METHODS: Male SD rats were randomly divided into the blank group, the model group, the ibuprofen group, the Lianhua Qingwen capsule group and the CHQW group (2, 4 and 8 g/kg, respectively). The LPS-induced acute lung injury (ALI) model in rats was established after pre-administration. The histopathological changes in the lung and the levels of inflammatory factors in bronchoalveolar lavage fluid (BALF) and serum of ALI rats were observed. The inflammation-related proteins toll-like receptor 4 (TLR4), inhibitory kappa B alpha (IκBα), phospho-IκBα (p-IκBα), nuclear-factor-kappa B (NF-κB), and NLR family pyrin domain containing 3(NLRP3) expression levels were measured by western blotting analysis and immunohistochemical analysis. The chemical composition of CHQW was identified by liquid chromatography-quadrupole-time of flight-mass spectrometry (LC-Q-TOF-MS). RESULTS: CHQW significantly ameliorated lung tissue pathological injury in LPS-induced ALI rats and decreased the release of inflammatory cytokines (interleukin-1ß, interleukin-17 and tumor necrosis factor-α) in BALF and serum. In addition, CHQW decreased the expression of TLR4, p-IκBα and NF-κB proteins, increased the level of IκBα, regulated the TLR4/NF-κB signaling pathway, and inhibited the activation of NLRP3. The chemical components of CHQW were analyzed by LC-Q-TOF-MS, and a total of 48 components were identified by combining information from the literature, mainly flavonoids, organic acids, lignans, iridoids and phenylethanoid glycosides. CONCLUSION: The results of this study showed that the pretreatment of CHQW had a strong protective effect on LPS-induced ALI in rats, reducing lung tissue lesions and decreasing inflammatory cytokines released in BALF and serum. The protective mechanism of CHQW may be related to the inhibition of the TLR4/NF-κB signaling pathway and NLRP3 activation. The main active ingredients of CHQW are flavonoids, organic acids, lignans, iridoids and phenylethanoid glycosides.

Eriobotrya japonica leaf triterpenoid acids ameliorate metabolic syndrome in C57BL/6J mice fed with high-fat diet.

BACKGROUND: It has been demonstrated in some studies that triterpenoid acid extract fromEriobotrya japonica leaf is beneficial to prevent hyperlipidemia or insulin resistance. However, the effect of triterpenoid acids in Eriobotrya japonica leaf on a series of typical symptoms of metabolic syndrome (MetS) has been rarely studied systematically. Therefore, the present study aims to systematically evaluate the effect of Eriobotrya japonica leaf triterpenoid acids (ELTA) on MetS and explore its potential mechanism. METHODS: ELTA (HPLC purity 95.2 %) was prepared and administered orally (200 mg/kg) to C57BL/6 J mice fed with a high-fat diet (HFD) for 12 weeks. Pioglitazone (30 mg/kg) was used as a positive control drug. Food intake, body weight, total lipid in feces, lipid profiles, inflammatory factors in serum, hepatic glutathione, and lipid peroxide were measured. Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed to evaluate insulin sensitivity. RT-qPCR and molecular docking were performed to explore the potential mechanism. RESULTS: ELTA administration reduced body weight gain, relative liver weight, and relative visceral adipose weight. The levels of serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, hepatic total cholesterol, and hepatic triglycerides were also reduced. ELTA reduced the area under curve (AUC) of blood glucose curves in OGTT and ITT. Relative mRNA level analysis of genes related to MetS showed that ELTA can effectively increase the transcriptional levels of Nrf2, HO-1, PPAR-γ, GluT2, GK, FXR, while effectively decrease those of PTP1B, p65, TNF-α, IL-6, SREBP, 11ßHSD-1. Molecular docking showed that the ligands in ELTA can bind to 11ßHSD-1, GK, PPAR-γ, and JNK, the important targets involved in MetS. CONCLUSIONS: ELTA can effectively alleviate visceral central obesity, insulin resistance, dyslipidemia, oxidative stress, and inflammation of HFD-induced MetS in C57BL/6 J mice. This is possibly achieved by acting on 11ßHSD-1, GK, PPAR-γ, and JNK.

Acute and Subacute Oral Toxicity Evaluation of Eriobotrya japonica Leaf Triterpene Acids in ICR Mice.

The interest focusing on Eriobotrya japonica leaf triterpene acid (ELTA) has increased recently because of its beneficial effects on health. However, there has been a lack of experimental data on its toxicity. The present study therefore was conducted to evaluate its toxicity in ICR mice. The results showed that ELTA produced neither mortality nor toxicity of the main organs in ICR male and female mice in both acute (0.30, 0.65, 1.39, and 3.00 g·kg-1 body weight) and subacute (150, 300, and 600 mg·kg-1 BW) 28-day toxicity studies. Because of lacking apparently adverse effects found in the hematology, clinical biochemistry, and histopathology evaluation, results of the present study together with the beneficial effects make ELTA as a promising dietary supplement and indicated that ELTA administered orally might have a large safety margin for human.

Protective effect of Astragalus polysaccharides on ATP binding cassette transporter A1 in THP-1 derived foam cells exposed to tumor necrosis factor-alpha.

Astragalus polysaccharide (APS), the main extract from the traditional Chinese medicinal herb Astragalus membranaceus, has been reported to benefit the treatment of immune-inflammatory diseases and metabolic disorders. In atherosclerotic plaques, proinflammatory cytokines exert adverse effects on lipids thereby aggravating atherosclerosis. Recent evidence shows that tumor necrosis factor-alpha (TNF-alpha) can down-regulate the expression of ATP-binding cassette transporter A1 (ABCA1), which plays a vital role in reverse cholesterol transport and determines the process of atherosclerosis. In the present study, the effects of APS on ABCA1 expression, cholesterol effluent rate and total cholesterol content of THP-1 derived foam cells exposed to TNF-alpha were investigated. Compared with the foam cells exposed to TNF-alpha, ABCA1 expression was promoted in the presence of APS. Consequently the cholesterol effluent rate increased and the total cholesterol content decreased significantly. TNF-alpha could enhance the activity of nuclear factor-kappa B (NF-kappaB) in the foam cells. This effect could be attenuated by APS. These findings suggest that APS could protect ABCA1 against the lesion of TNF-alpha in THP-1 derived foam cells, which may contribute to its antiatherosclerotic properties.