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Background: Sodium new houttuyfonate (SNH) has been reported to have anti-inflammatory, anti-fungal, and anti-cancer effects. However, few studies have investigated the effect of SNH on breast cancer. The aim of this study was to investigate whether SNH has therapeutic potential for targeting breast cancer. Methods: Immunohistochemistry and Western blot analysis were used to examine the expression of proteins, flow cytometry was used to detect cell apoptosis and ROS levels, and transmission electron microscopy was used to observe mitochondria. Results: Differentially expressed genes (DEGs) between breast cancer-related gene expression profiles (GSE139038 and GSE109169) from GEO DataSets were mainly involved in the immune signaling pathway and the apoptotic signaling pathway. According to in vitro experiments, SNH significantly inhibited the proliferation, migration, and invasiveness of MCF-7 (human cells) and CMT-1211 (canine cells) and promoted apoptosis. To explore the reason for the above cellular changes, it was found that SNH induced the excessive production of ROS, resulting in mitochondrial impairment, and then promoted apoptosis by inhibiting the activation of the PDK1-AKT-GSK3β pathway. Tumor growth, as well as lung and liver metastases, were suppressed under SNH treatment in a mouse breast tumor model. Conclusions: SNH significantly inhibited the proliferation and invasiveness of breast cancer cells and may have significant therapeutic potential in breast cancer.

Background. Persistent endometritis caused by bacterial infections has lethal effects on the reproductive performance of dairy cattle, which compromises animal welfare and delays or prevents pregnancy. The microRNA (miRNA) miR-34 family plays a pivotal role in the inflammatory process; however, the precise mechanism of miR-34a in endometritis has not been thoroughly elucidated to date. Methods. In this study, the endometrium of cows diagnosed with endometritis was harvested for bacterial culture and Gram staining to evaluate bacterial contamination of the uterus. Based on this, a bovine endometrial epithelial cell (BEND) inflammation model and a mouse model stimulated with lipopolysaccharide (LPS) in vitro and in vivo were constructed. Cell viability was assessed by CCK-8, trypan blue staining, and flow cytometry. H&E was applied to histopathological analysis. Immunohistochemical, immunofluorescence, qRT-PCR, and western blot assays were performed to measure the mRNA and protein expression of relevant genes. Online databases, plasmid construction, and dual-luciferase reporter gene assays were used to predict and validate the interaction between miR-34a and its target gene LGR4. Finally, mice were injected vaginally with a local antagomir to validate the role of miR-34a in murine uterine inflammation. Results. In this study, we observed that Gram-negative bacteria, represented by Escherichia coli, are the predominant pathogenic agents responsible for the recurrent occurrence of endometritis in dairy cows. Further, miR-34a was found to repress the expression of LGR4 by targeting the 3 ′ untranslated region (3 ′ UTR) of LGR4. miR-34a was upregulated in bovine uterine tissues and bovine endometrial epithelial cells stimulated with LPS. miR-34a induced the release of the proinflammatory cytokines IL-1β, IL-6, and TNF-α by activating the phosphorylation of NF-κB p65. Furthermore, IL-1β upregulated miR-34a transcription and downregulated LGR4 expression in an IL-1β-dependent manner. Conclusions. Taken together, our study confirmed that miR-34a is regulated by IL-1β and suppresses the level of the LGR4 3 ′ UTR, which in turn exacerbates the inflammatory response. Thus, the knockdown of miR-34a might be a new direction for the treatment of endometritis.

Endometritis is a severe postpartum inflammatory disease that puts cows' reproductive health at risk and causes the dairy industry to suffer significant financial losses. The present study aimed to investigate the regulatory role of miR‑26a in LPS‑induced bovine endometrial epithelial cells (bEECs) and the implication for endometritis. Here, we found inflammatory cell infiltration and destruction of endometrial structure in cow uterus, and dramatic increase in myeloperoxidase (MPO) activity and upregulation of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) in endometritis. Meanwhile, miR-26a was down-regulated, but MAP3K8 was increased in the uterine tissue of endometritis. Similarly, the expression of miR-26a was significantly decreased in LPS-stimulated bEECs, while MAP3K8 was risen. In addition, we further verified that MAP3K8 was a target of miR-26a by dual-luciferase reporter assay. Under LPS stress, over-expressing miR-26a markedly decreased MAP3K8 expression levels, along with the reduced expression of inflammatory factors, such as IL-1β, TNF-α and IL-6, whereas this effect was countered by the inhibition of miR-26a. Furthermore, we demonstrated that miR-26a overexpression prevented the MAPK pathway from being activated by targeting MAP3K8. Then we carried out experiments in LPS-stimulated mice uterus to expound that MAP3K8 was essential in endometritis development, which further confirmed the reliability of the above results. In conclusion, overexpression of miR-26a effectively inhibited the expression of MAP3K8 in LPS-induced bEECs and thereby partially suppressed the activation of MAPK signaling pathway. miR-26a and MAP3K8 may be a promising biomarker and therapeutic target for dairy cow endometritis.

Mastitis, caused by a variety of pathogenic microorganisms, seriously threatens the safety and economic benefits of the dairy industry. Vitexin, a flavone glucoside found in many plant species, has been widely reported to have antioxidant, anti-inflammatory, antiviral, anticancer, neuroprotective, and cardioprotective effects. However, few studies have explored the effect of vitexin on mastitis. This study is aimed at exploring whether the antioxidant and anti-inflammatory functions of vitexin can improve Staphylococcus aureus-induced mastitis and its possible molecular mechanism. The expression profiles of S. aureus-infected bovine mammary epithelial cells and gland tissues from the GEO data set (GSE94056 and GSE139612) were analyzed and found that DEGs were mainly involved in immune signaling pathways, apoptosis, and ER stress through GO and KEGG enrichment. Vitexin blocked the production of ROS and increased the activity of antioxidant enzymes (SOD, GSH-PX, and CAT) via activation of PPAR

Mastitis, caused by a variety of pathogenic microorganisms, seriously threatens the safety and economic benefits of the dairy industry. Vitexin, a flavone glucoside found in many plant species, has been widely reported to have antioxidant, anti-inflammatory, antiviral, anticancer, neuroprotective, and cardioprotective effects. However, few studies have explored the effect of vitexin on mastitis. This study is aimed at exploring whether the antioxidant and anti-inflammatory functions of vitexin can improve Staphylococcus aureus-induced mastitis and its possible molecular mechanism. The expression profiles of S. aureus-infected bovine mammary epithelial cells and gland tissues from the GEO data set (GSE94056 and GSE139612) were analyzed and found that DEGs were mainly involved in immune signaling pathways, apoptosis, and ER stress through GO and KEGG enrichment. Vitexin blocked the production of ROS and increased the activity of antioxidant enzymes (SOD, GSH-PX, and CAT) via activation of PPARγ in vivo and in vitro. In addition, vitexin reduced the production of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and inhibited apoptosis in MAC-T cells and mouse mammary tissues infected with Staphylococcus aureus. Moreover, vitexin decreased the expression of PDI, Ero1-Lα, p-IRE1α, PERK, p-eIF2α, and CHOP protein but increased BiP in both mammary gland cells and tissues challenged by S. aureus. Western blot results also found that the phosphorylation levels of JNK, ERK, p38, and p65 were reduced in vitexin-treated tissues and cells. Vitexin inhibited the production of ROS through promoting PPARγ, increased the activity of antioxidant enzymes, and reduced inflammatory cytokines and apoptosis by alleviating ER stress and inactivation MAPKs and NF-κB signaling pathway. Vitexin maybe have great potential to be a preventive and therapeutic agent for mastitis.

Endometritis is inflammation of endometrium due to various factors and is a common cause of infertility. Several remedies used for endometritis like antibiotics, hormones, and herbs. Studies confirm that microRNAs play a significant role in various inflammatory diseases. However, the role of miR-424-5p in endometritis is not clear. In our study, histopathology, real-time quantitative polymerase chain reaction, Western blot analysis, immunofluorescence, ELISA, and dual-luciferase reporter assay were used to elucidate the effect of miR-424-5p in lipopolysaccharide (LPS)-primed inflammatory response in bovine endometrial epithelial cells (BEECs) and clarify the potential mechanism. Our results revealed that miR-424-5p mimics noticeably decrease the production of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), while miR-424-5p inhibitors have inverse effects in BEECs. Moreover, overexpression of miR-424-5p on BEECs cells also suppressed NF-κB p65 activation. Afterwards, we verified that miR-424-5p inhibited Interleukin 1 Receptor Associated Kinase 2 (IRAK2) expression by binding to the 3'-UTR of IRAK2 mRNA. Further, co-transfection of miR-424-5p inhibitors and siRNA-IRAK2 revealed that negative regulation of miR-424-5p on LPS-induced inflammatory response in BEECs was mediated by IRAK2.Mutually, miR-424-5p pharmacologic stabilization represents an entirely unique medical aid for cow endometritis and other inflammation-related diseases.

Background Persistent endometritis caused by bacterial infections has lethal effects on the reproductive performance of dairy cattle, which compromises animal welfare and delays or prevents pregnancy. The microRNA (miRNA) miR-34 family plays a pivotal role in the inflammatory process; however, the precise mechanism of miR-34a in endometritis has not been thoroughly elucidated to date. Methods In this study, the endometrium of cows diagnosed with endometritis was harvested for bacterial culture and Gram staining to evaluate bacterial contamination of the uterus. Based on this, a bovine endometrial epithelial cell (BEND) inflammation model and a mouse model stimulated with lipopolysaccharide (LPS) in vitro and in vivo were constructed. Cell viability was assessed by CCK-8, trypan blue staining, and flow cytometry. H&E was applied to histopathological analysis. Immunohistochemical, immunofluorescence, qRT-PCR, and western blot assays were performed to measure the mRNA and protein expression of relevant genes. Online databases, plasmid construction, and dual-luciferase reporter gene assays were used to predict and validate the interaction between miR-34a and its target gene LGR4. Finally, mice were injected vaginally with a local antagomir to validate the role of miR-34a in murine uterine inflammation. Results In this study, we observed that Gram-negative bacteria, represented by Escherichia coli, are the predominant pathogenic agents responsible for the recurrent occurrence of endometritis in dairy cows. Further, miR-34a was found to repress the expression of LGR4 by targeting the 3′ untranslated region (3′UTR) of LGR4. miR-34a was upregulated in bovine uterine tissues and bovine endometrial epithelial cells stimulated with LPS. miR-34a induced the release of the proinflammatory cytokines IL-1β, IL-6, and TNF-α by activating the phosphorylation of NF-κB p65. Furthermore, IL-1β upregulated miR-34a transcription and downregulated LGR4 expression in an IL-1β-dependent manner. Conclusions Taken together, our study confirmed that miR-34a is regulated by IL-1β and suppresses the level of the LGR4 3′UTR, which in turn exacerbates the inflammatory response. Thus, the knockdown of miR-34a might be a new direction for the treatment of endometritis.

Background Persistent endometritis lead by bacterial infections has lethal effects on the reproductive performance of dairy cattle, which not only compromise animal welfare but also delay or prevent pregnancy. MicroRNA (miRNA) miR-34 family plays a pivotal role in the inflammatory process; however, the precise mechanism of miR-34a in endometritis is still not thoroughly revealed. Methods In this study, we established bovine endometrial epithelial cell (BENDs) inflammation model and mouse model stimulation with Lipopolysaccharide (LPS) in vitro and in vivo. CCK-8 was used to assess cell viability. H&E was used to characterize morphology. Immunohistochemistry, immunofluorescence, qRT-PCR and western blot assays were performed to measure the mRNA or protein expression of related genes. Online database, plasmid construction and dual-luciferase Reporter gene assays were applied to predict and validate the interaction between miR-34a and its target gene LGR4, and mice were injected vaginally with local antagomir to validate the role of miR-34a in murine uterine inflammation. Results Here, we report that miR-34a suppresses LGR4 gene expression by targeting its 3'untranslated regions (3'UTR). The miR-34a was up-regulated in cow uterine tissues and bovine endometrial epithelial cell (BENDs) stimulation with LPS. It further induces the release of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α by activating the phosphorylation level of NF-κB p65. Furthermore, we also revealed that IL-1β was responsible for the upregulation of miR-34a transcription and downregulation of LGR4 in an IL-1β-dependent manner. Conclusions Taken together, our study confirmed that miR-34a is regulated by IL-1β and suppress the level of LGR4 3’UTR which in turn exacerbates the inflammatory response. Thus knockdown miR-34a might be a new indirection for treatment endometritis.

Solving the reproductive barriers of dairy cows has become one of the most critical factors determining the dairy industry's development. Clinically, inflammation disease like endometritis is the most crucial cause in reducing dairy production's financial viability. MiR-193 family can induce cell apoptosis and differentiation has been reported in various diseases. LGR4 plays a vital role in reproductive system development and immune system regulation, and it is closely related to animal reproductive function and cytokine regulation. In this study, we observed a negative relationship between miR-193a-3p and LGR4 expression level in both inflammatory tissues and cells. The expression level of miR-193a-3p and LGR4 in bovine endometrial epithelial cells (BENDs) is regulated by lipopolysaccharide (LPS) stimulation time and dose-dependent. Subsequently, miR-193a-3p mimics and inhibitors were used to explore its functions in the inflammation response process, finding that overexpression of miR-193a-3p markedly increases the expression level of pro-inflammatory cytokines induced by LPS, such as IL-1β, IL-6 and TNF-α, while the group in which transfected inhibitor is on the contrary. Of note, immunofluorescence and western blot results showed that miR-193a-3p enhanced LPS-induced NF-κB p65 phosphorylation through targeting LGR4, whereas inhibiting miR-193a-3p could suppress the activation of NF-κB pathway significantly. In conclusion, our study firstly reported the mechanism by which miR-193a-3p targets LGR4 to elevate the inflammatory response in bovine endometrium injury, thereby implying that knockdown miR-193a-3p may lay the theoretical and practical basis for drug development of alleviating endometritis in dairy cows.

Endometritis in dairy cows is a major economic problem worldwide; without advances in lifestyle management and drug treatment, it causes high morbidity and death. Micro ribonucleic acid (miRNAs) these days is seen as an important part of gene control networks. It is a class of small nucleotides 20-25, single-stranded RNA molecules. In endometritis, the inflammatory response caused by the gram-negative bacteria Escherichia coli (E. coli) alters the expression of miRNA which can regulate the innate immune system. This manuscript reviews (1) the interaction of miRNAs with the signaling of NF-κB and dysregulation of miRNAs and NF-κB activity in endometritis and (2) the activity of miR-let-7c, miR-148a, and miR-488 in NF-κB activation and their effect on endometritis. Cows with reduced immunity are more vulnerable to transition diseases, such as endometritis. During post-partum, cows undergo stress, metabolic disorders, hormonal imbalance, negative energy balance, and changes in diet. One of the many categories of regulatory molecules, which explain its natural function and pathological impact on NF-κB dysregulation, is important to inform the complexity of the immune system and to develop treatments for endometritis. It shows that miRNAs could have multiple applications in veterinary medicine. Nevertheless, a comprehensive study of is essential which should be aimed at exploring the role of microRNA at physiological level and its effect due to dysfunction and dysregulation.

Acute lung injury (ALI) is considered as an uncontrolled inflammatory response that can leads to acute respiratory distress syndrome (ARDS), which limits the therapeutic strategies. Ginsenosides Rb1 (Rb1), an active ingredient obtained from Panax ginseng, possesses a broad range of pharmacological and medicinal properties, comprising the anti-inflammatory, anti-oxidant, and anti-tumor activities. Therefore, the purpose of the present study was to investigate the protective effects of Rb1 against S. aureus-induced (ALI) through regulation of Nuclear factor erythroid 2-related factor 2 (Nrf2) and mitochondrial-mediated apoptotic pathways in mice (in-vivo), and RAW264.7 cells (in-vitro). For that purpose, forty Kunming mice were randomly assigned into four treatment groups; (1) Control group (phosphate buffer saline (PBS); (2) S. aureus group; (3) S. aureus + Rb1 (20 mg/kg) group; and (4) Rb1 (20 mg/kg) group. The 20 μg/mL dose of Rb1 was used in RAW264.7 cells. In the present study, we found that Rb1 treatment reduced ALI-induced oxidative stress via suppressing the accumulation of malondialdehyde (MDA) and myeloperoxidase (MPO) and increase the antioxidant enzyme activities of superoxidase dismutase 1 (SOD1), Catalase (CAT), and glutathione peroxidase 1 (Gpx1). Similarly, Rb1 markedly increased messenger RNA (mRNA) expression of antioxidant genes (SOD1, CAT and Gpx1) in comparison with ALI group. The histopathological results showed that Rb1 treatment ameliorated ALI-induced hemorrhages, hyperemia, perivascular edema and neutrophilic infiltration in the lungs of mice. Furthermore, Rb1 enhanced the antioxidant defense system through activating the Nrf2 signaling pathway. Our findings showed that Rb1 treated group significantly up-regulated mRNA and protein expression of Nrf2 and its downstream associated genes down-regulated by ALI in vivo and in vitro. Moreover, ALI significantly increased the both mRNA and protein expression of mitochondrial-apoptosis-related genes (Bax, caspase-3, caspase-9, cytochrome c and p53), while decreased the Bcl-2. In addition, Rb1 therapy significantly reversed the mRNA and protein expression of these mitochondrial-apoptosis-related genes, as compared to the ALI group in vivo and in vitro. Taken together, Rb1 alleviates ALI-induced oxidative injury and apoptosis by modulating the Nrf2 and mitochondrial signaling pathways in the lungs of mice.

Hederacoside-C (HDC) is a biological active ingredient, extracted from the leaves of Hedera helix. It has been reported to have anti-inflammatory properties. However, the effects of HDC on Staphylococcus aureus (S. aureus)-induced mastitis have not been reported yet. Here, we evaluated the anti-inflammatory effects of HDC on S. aureus-induced mastitis both in vivo on mammary gland tissues and in vitro on RAW 264.7 cells. The ascertained histopathological changes and MPO activity revealed that HDC defended mammary glands from tissue destruction and inflammatory cell infiltration induced by S. aureus. The results of ELISA, western blot, and qRT-PCR indicated that HDC significantly inhibited the expressions IL-6, IL-1β, and TNF-α and enhanced the IL-10 by downregulating and upregulating their relevant genes, respectively. Furthermore, HDC markedly suppressed the TLR2 and TLR4 expressions by attenuating the MAPKs (p38, ERK, JNK) and NF-κB (p65 and IκBα) pathways followed by decreasing the phosphorylation of p38, ERK, JNK, p65, and IκBα. The above parameters enhanced the mammary gland defense and reduced inflammation. These findings suggested that HDC may have the potential to be an effective anti-inflammatory drug for the S. aureus-induced mice mastitis and in RAW 264.7 cells.

Mastitis is the inflammation of mammary glands which causes huge economic loss in dairy cows. Inflammation, any tissue injury and pathogens in cow udder activate Toll-like Receptors (TLRs). Staphylococcus aureus (S. aureus) is the major cause of mastitis. In mastitis, activated TLRs initiate the NF-κB/MAPKs pathways which further trigger the gene expression associated with mastitis followed by innate immune response. In this study, pathogenic-induced gene expression profile of pro-inflammatory cytokines in mammary gland tissues, was investigated in mastitis. The Hematoxylin and Eosin (H & E) results indicated severe histopathological changes in infected tissues. Western blot results suggested the over expressions of TLR2/TLR4 with NF-κB/MAPKs pathways activation in infected tissues. qRT-PCR results revealed the gene expression associated with TLR2/TLR4-mediated NF-κB/MAPKs pathways in infected tissues in comparison with non-infected. Statistical analysis of mRNA and relative protein expression levels indicated the up-regulation of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in infected tissues rather than non-infected tissues. These results suggested that the up-regulation of gene expression levels implicated the underlying regulatory pathways for proper immune function in mammary glands. In conclusion, our study might give new insights for investigation and better understanding of mammary gland pathophysiology and TLRs and NF-κB/MAPKs-mediated gene expression of pro-inflammatory cytokines.

Objective Staphylococcus aureus (S. aureus), one of Gram-positive pathogen, is frequently associated with acute lung inflammation. The central feature of S. aureus acute lung inflammation are pulmonary dysfunctioning and impeded host defence response, which cause failure in inflammatory cytokines homeostasis and leads to serious tissue damage. However, the role of the Mer receptor tyrosine kinase (MerTK) in the lung following S. aureus infection remains elusive. Here, we investigate whether MerTK alleviates S. aureus induced uncontrolled inflammation through negatively regulating toll-like receptor 2 and 6 (TLR2/ TLR6) via suppressor of cytokine signalling 1, 3 (SOCS1/SOCS3). Methods and results We found in mice lung tissues and RAW 264.7 macrophages upon S. aureus infection activates TLR2 and TLR6 driven mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) signalling pathways, resulting in production of inflammatory cytokines including tumour necrosis factor-α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6). Furthermore, S. aureus-infection groups showed a significant up-regulation of MerTK which serves as mediator of SOCS1 and SOCS3. Subsequently, through feedback mechanism SOCS1/3 degrade Mal, resulting in inhibition of downstream TLR mediated inflammatory pathways. Moreover, MerTK−/− mice lung tissues and silencing MerTK in RAW 264.7 inhibited the S. aureus-induced activation of MerTK, which significantly upregulated the phosphorylation of crucial protein in MAPKs (ERK, JNK, p38) and NF-κB (IĸBα, p65) signalling pathways, as well as the production of pro-inflammatory cytokines. Conclusion Collectively, these findings indicate the important role of MerTK in self-regulatory resolution of S. aureus-induced inflammatory pathways and cytokines through intrinsic SOCS1 and SOCS3 repressed feedback on TLR2, TLR6 both in vivo and in vitro.

Acute lung injury (ALI) is clinically characterized by excessive inflammation leading to acute respiratory distress syndrome (ARDS), having high morbidity and mortality both in human and animals. Ginsenoside Rb1 (Rb1) is a major primary bioactive component extracted by Panax ginseng, which has numerous pharmacological functions such as anti-cancer, anti-inflammatory, and antioxidant. However, the anti-inflammatory effects of Rb1 in Staphylococcus aureus (S. aureus)-induced ALI in mice have not been investigated. The aim of the current study was to determine the anti-inflammatory influence of Rb1 on S. aureus-induced ALI in mice, and to explore its possible underlying principle mechanisms in RAW 264.7 macrophage cells. The results of physical morphology, histopathological variation and wet-to-dry weight ratio of lungs revealed that Rb1 significantly attenuated S. aureus-induced lung injury. Furthermore, qPCR results displayed that Rb1 inhibited IL-1β, IL-6 and TNF-α production both in vivo and in vitro. The activation of Toll-like receptor 2 (TLR2) by S. aureus was inhibited by application of Rb1 as confirmed by results of immunofluorescence assay. The expression of NF-kB and MAPK signaling proteins revealed that Rb1 significantly attenuated the phosphorylation of p65, ERK, as well as JNK. Altogether, the results of this experiment presented that Rb1 has ability to protect S. aureus-induced ALI in mice by attenuating TLR-2-mediated NF-kB and MAPK signaling pathways. Consequently, Rb-1 might be a potential medicine in the treatment of S. aureus-induced lung inflammation.

Acute lung inflammation is one among the top of infectious diseases. It is a pulmonary dysfunctional disease. It breaks the physiological coordination in the structures and functions of respiratory system. There are a few effective treatments to minimize the mortality of acute lung inflammation. It was induced by Staphylococcus aureus (S. aureus) via nasal instillation of mice. The common ivy (Hedera helix) is the most significant medicinal plant and considered as a traditional medicinal plant. The most active ingredient in the extract of ivy plant was Hederacoside-C (HDC). The purpose of this study was to investigate its anti-inflammatory effects on induced acute lung inflammation in vivo and (RAW 264.7 cells) in vitro and to elucidate its anti-inflammatory mechanisms. HDC was administered intraperitoneally 1 h after infection until 24 h. The dose was repeated every 8 h for three successful doses. Mice treated with HDC significantly reduced the pulmonary edema, white blood cells, wet-dry ratio (W/D) and myeloperoxidase (MPO) activity. HDC attenuated protein expression levels of MAPKs including p38, ERK, JNK and NF-κB including p65 and IκB-α pathways analyzed by ELISA. HDC also suppressed the protein expressions of TLR2 & TLR4 detected by Western blot. HDC also downregulated the gene expression of pro-inflammatory cytokines including IL-6, IL-1β and TNF-α, but upregulated the gene expression of an anti-inflammatory cytokine IL-10 analyzed by qRT-PCR. In conclusion, our results stated that HDC could inhibit the S. aureus induced acute lung inflammation and it may be a potential therapeutic drug against acute lung inflammation.