Preparation, characterisation and in vitro anti-inflammatory activity of Baicalin microsponges.

Baicalin, a flavonoid extracted from traditional Chinese medicine, Scutellaria baicalensis has significant anti-inflammatory effects. Microsponges are drug delivery systems that improve drug stability and slow the release rate. The combination of baicalin and the microsponges produced a new and stable system for its delivery, resulting in a novel formulation of baicalin. Baicalin microsponges (BM) were prepared using the quasi-emulsion solvent diffusion method. Effects of the mass ratio of the polymer (ethylcellulose) to baicalin, the concentration of the emulsifier polyvinyl alcohol (PVA), the stirring speed on the encapsulation efficiency (EE), and yield of the microsponges were investigated by combining the one-factor test and Box-Behnken design (BBD). The preparation process was standardised using 2.61:1 mass ratio of ethyl cellulose to baicalin, 2.17% concentration of PVA, with stirring at 794 rpm. Optimised BM formulations were evaluated for the parameters of EE (54.06 ± 3.02)% and yield of (70.37 ± 2.41)%, transmission electron microscopy (TEM), and in vitro cell evaluation. Results of the in vitro anti-inflammatory assay showed that baicalin microsponges-pretreated-lipopolysaccharide (LPS)-induced RAW264.7, mouse macrophages showed reduced inflammatory response, similar to that seen in baicalin-treated macrophages.

Gypenoside XLIX alleviates acute liver injury: Emphasis on NF-κB/PPAR-α/NLRP3 pathways.

Liver is one of the vital organs in the human body and liver injury will have a very serious impact on human damage. Gypenoside XLIX is a PPAR-α activator that inhibits the activation of the NF-κB signaling pathway. The components of XLIX have pharmacological effects such as cardiovascular protection, antihypoxia, anti-tumor and anti-aging. In this study, we used cecum ligation and puncture (CLP) was used to induce in vivo mice hepatic injury, and lipopolysaccharide (LPS)-induced inflammation in RAW264.7 cells, evaluated whether Gypenoside XLIX could have a palliative effect on sepsis-induced acute liver injury via NF-κB/PPAR-α/NLRP3. In order to gain insight into these mechanisms, six groups were created in vivo: the Contol group, the Sham group, the CLP group, the CLP + XLIX group (40 mg/kg) and the Sham + XLIX (40 mg/kg) group, and the CLP + DEX (2 mg/kg) group. Three groups were created in vitro: Control, LPS, LPS + XLIX (40 µM). The analytical methods used included H&E staining, qPCR, reactive oxygen species (ROS), oil red O staining, and Western Blot. The results showed that XLIX attenuated hepatic inflammatory injury in mice with toxic liver disease through inhibition of the TLR4-mediated NF-κB pathway, attenuated lipid accumulation through activation of PPAR-α, and attenuated hepatic pyroptosis by inhibiting NLRP3 production. Regarding the imbalance between oxidative and antioxidant defenses due to septic liver injury, XLIX reduced liver oxidative stress-related biomarkers (ALT, AST), reduced ROS accumulation, decreased the amount of malondialdehyde (MDA) produced by lipid peroxidation, and increased the levels of antioxidant enzymes such as glutathione (GSH) and catalase (CAT). Our results demonstrate that XLIX can indeed attenuate septic liver injury. This is extremely important for future studies on XLIX and sepsis, and provides a potential pathway for the treatment of acute liver injury.

Quercetin alleviates the toxicity of difenoconazole to the respiratory system of carp by reducing ROS accumulation and maintaining mitochondrial dynamic balance.

Difenoconazole (DFZ) is a fungicidal pesticide extensively employed for the management of fungal diseases in fruits, vegetables, and cereal crops. However, its potential environmental impact cannot be ignored, as DFZ accumulation is able to lead to aquatic environment pollution and harm to non-target organisms. Quercetin (QUE), a flavonoid abundant in fruits and vegetables, possesses antioxidant and anti-inflammatory properties. In this article, carp were exposed to 400 mg/kg QUE and/or 0.3906 mg/L DFZ for 30 d to investigate the effect of QUE on DFZ-induced respiratory toxicity in carp. Research shows that DFZ exposure increases reactive oxygen species (ROS) production in the carp's respiratory system, leading to oxidative stress, inflammation, and damage to gill tissue and tight junction proteins. Further research demonstrates that DFZ induces mitochondrial dynamic imbalance and gill cell apoptosis. Notably, QUE treatment significantly reduces ROS levels, alleviates oxidative stress and inflammation, and mitigates mitochondrial dynamics imbalance and mitochondrial apoptosis. This study emphasizes the profound mechanism of DFZ toxicity to the respiratory system of common carp and the beneficial role of QUE in mitigating DFZ toxicity. These findings contribute to a better understanding of pesticide risk assessment in aquatic systems and provide new insights into strategies to reduce their toxicity.

Monotropein induces autophagy through activation of the NRF2/PINK axis, thereby alleviating sepsis-induced colonic injury.

Sepsis is a systemic inflammatory disease that is caused by a dysregulated host response to infection and is a life-threatening organ dysfunction that affects many organs, which includes the colon. Mounting evidence suggests that sepsis-induced colonic damage is a major contributor to organ failure and cellular dysfunction. Monotropein (MON) is the major natural compound in the iris glycoside that is extracted from Morendae officinalis radix, which possesses the potent pharmacological activities of anti-inflammatory and antioxidant properties. This research evaluated whether MON is able to alleviate septic colonic injury in mice by cecal ligation and puncture. Colonic tissues were analyzed using histopathology, immunofluorescence, quantitative real-time polymerase chain reaction, and Western blot methods. It was initially discovered that MON reduced colonic damage in infected mice, in addition to inflammation, apoptosis, and oxidative stress in colonic tissues, while it activated autophagy, with the NRF2/keap1 and PINK1/Parkin pathways also being activated. Through the stimulation of NCM460 cells with lipopolysaccharides, an in vitro model of sepsis was created as a means of further elucidating the potential mechanisms of MON. In the in vitro model, it was found that MON could still activate the NRF2/keap1, PINK1/Parkin, and autophagy pathways. However, when MON was paired with the NRF2 inhibitor ML385, it counteracted MON-induced activation of PINK1/Parkin and autophagy, while also promoting inflammatory response and apoptosis in NCM460 cells. Therefore, the data implies that MON could play a therapeutic role through the activation of the NFR2/PINK pathway as a means of inducing autophagy to alleviate the oxidative stress in colonic tissues that is induced by sepsis, which will improve inflammation and apoptosis in colonic tissues.

Gypenoside XLIX attenuates sepsis-induced splenic injury through inhibiting inflammation and oxidative stress.

BACKGROUND: To investigate the effect of Gypenoside XLIX (Gyp-XLIX) on acute splenic injury (ASI) induced by cecal ligation and puncture (CLP) in septic mice, a study was conducted. METHODS: Sixty healthy mice were randomly divided into six groups: the NC group, the Sham group, the Sham + Gyp-XLIX group, the CLP group, the CLP + Gyp-XLIX group, and the CLP + Dexamethasone (DEX) group. The NC group did not undergo any operation, while the rest of the groups underwent CLP to establish the sepsis model. The Sham group only underwent open-abdominal suture surgery without cecum puncture. After the operation, the groups were immediately administered the drug for a total of 5 days. Various methods such as hematoxylin and eosin (HE) staining, biochemical kits, qRT-PCR, and reactive oxygen species (ROS) were used for analysis. RESULTS: The results demonstrated that Gyp-XLIX effectively mitigated the splenic histopathological damage, while reducing the malondialdehyde (MDA) lipid peroxidation index and enhancing the antioxidant activities of catalase (CAT), glutathione (GSH) and total antioxidant capacity (T-AOC). The utilization of Dihydroethidium (DHE) fluorescent probe revealed that Gyp-XLIX inhibited the acute splenic accumulation of ROS induced by CLP in septic mice. Further investigations revealed that Gyp-XLIX exhibited a down-regulatory effect on the protein levels of inflammatory mediators iNOS and COX-2, consequently leading to the suppression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1ß. Additionally, it up-regulated the expression of anti-inflammatory factor IL-10. CONCLUSION: In conclusion, Gyp-XLIX was significantly effective in attenuating CLP-induced acute splenic inflammation and oxidative stress in septic mice.

Mitigation of avermectin exposure-induced brain tissue damage in carp by quercetin.

Avermectin is widely used as an important insecticide in agricultural production, but it also shows strong toxicity to non-target organisms. Quercetin is a natural flavonoid that is widely used due to its good anti-inflammatory and antioxidant effects. We believe that quercetin may have a potential therapeutic effect on avermectin poisoning. This experiment was proposed to observe the effect of quercetin on the toxic response to avermectin by observing the toxic response caused by avermectin in the brain of carp. In this project, 60 carp were studied as control group (Control), quercetin administration group (QUE), avermectin exposure group (AVM) and quercetin treatment avermectin exposure group (QUE + AVM) with different interventions to study the effect of quercetin on avermectin. The carp brain tissues were stained and simultaneously analyzed for blood-brain barrier (BBB), oxidative stress indicators, inflammatory factors, and apoptosis using qPCR technique. The results of the study indicate that avermectin exhibits a neurotoxic mechanism of action in fish by decreasing the transcript levels of tight junction protein-related genes, which in turn leads to the rupture of the BBB in the carp brain tissue. Avermectin induced apoptosis in carp brain tissue by increasing oxidative stress response and promoting inflammatory cell infiltration. Quercetin could reduce the accumulation of reactive oxygen species (ROS) in the brain tissue of carp caused by avermectin exposure toxicity, maintain redox homeostasis, reduce inflammatory response, and protect brain tissue cells from apoptosis. The present study confirmed the therapeutic and protective effects of quercetin on neurotoxicity in carp caused by avermectin exposure.

Quercetin attenuates environmental Avermectin-induced ROS accumulation and alleviates gill damage in carp through activation of the Nrf2 pathway.

Avermectin (AVM) is one of the most often used insecticides which is toxic to aquatic organisms, and cause oxidative-induced damages to the fish respiratory organ, the "gills". To better understand the mechanism by which an antioxidant reduces AVM-induced gill damage, we investigated the effects of Quercetin (Que) on AVM induction of oxidative stress to inhibit damages to the gills using common carp as a model organism. The Que is a fruit and vegetable rich flavonoid with antioxidant activity. In this study, four groups were created: the Control group, the Que group (400 mg/kg), the AVM group (2.404 µg/L), and the Que plus AVM group. The analytical methods were pathological structure examination, qPCR, Reactive Oxygen Species (ROS) and Western blot. The results showed that Que alleviated AVM-induced oxidative stress, inflammatory damage and apoptosis in the carp gills by activating the Nrf2 pathway. The mechanism was that Que alleviated the accumulation of ROS, reduced the balance between oxidation and antioxidant disrupted by AVM exposure, lowered the content of lipid peroxidation produced malondialdehyde (MDA), and increased the content of antioxidant enzymes including glutathione (GSH) and catalase (CAT). Nrf2 pathway was activated. Meanwhile, Que inhibited gill apoptosis in carp by decreasing the levels of Bax, Cytochrome C, Caspase9, Cleaved-Caspase3 and reduced Bcl2. This has important implications for future studies on Que and AVM. New suggestions are provided to reduce the threat of aquatic environmental pollution.

Quercetin attenuates avermectin-induced cardiac injury in carp through inflammation, oxidative stress, apoptosis and autophagy.

As an important antibiotic, avermectin (AVM) has been widely used in China, but its unreasonable application has caused serious harm to the water environment. In view of the various pharmacological effects of quercetin (QUE), such as anti-inflammatory and antioxidant, the scientific hypothesis that "QUE may cause carp poisoning by inhibiting AVM" was proposed in this study. However, its protective effect in AVM -induced heart damage has not been reported. QUE reduced the symptoms of AVM toxicity and decreased the levels of creatine kinase, lactate dehydrogenase, and creatine kinase in the serum of carp. By histological observation, QUE was found to significantly reduce cardiac fiber swelling in carp. A DHE fluorescence probe study showed that QUE was able to inhibit AVM -induced accumulation of reactive oxygen species (ROS) in carp myocardium. We found that QUE significantly increased the intracellular antioxidant enzymes CAT, T-AOC and GSH enzyme activity and reduced intracellular MDA content. In addition, QUE significantly increased il-10 and tgf-ß1 expression, and significantly down-regulated tnf-α, il-6, il-1ß and inos expression. Tunel assay showed that QUE attenuated AVM -induced apoptosis, significantly decreased the transcript levels of pro-apoptosis-related genes, and increased the expression of anti-apoptosis-related genes. We also detected the protein expression of LC3 in the AVM group and QUE + AVM group, and found that the expression of LC3 was significantly increased in both groups compared with the Control group, but after adding QUE, the expression of LC3 was significantly decreased compared with the AVM group. In addition, the transcript levels of p62 and atg5 were also detected by qPCR. QUE significantly increased the expression of p62 and decreased the expression of atg5, suggesting that QUE could attenuate AVM -induced cardiac autophagy in carp. This study will provide preliminary evidence of the principle of QUE attenuating AVM -induced myocardial injury in carp from four aspects, including oxidative stress, inflammatory response, apoptosis and autophagy, and provide a theoretical basis for its prevention and treatment.

Ameliorative Effect of Malvidin on Spleen Injury in LPS-Induced Sepsis.

Sepsis, one of the most destructive diseases in the world, is a syndrome of systemic inflammatory response caused by the invasion of pathogenic microorganisms such as bacteria into the body. Malvidin is one of the most widespread anthocyanins, and its significant antioxidant and anti-inflammatory activities have been widely reported. However, the effect of Malvidin on sepsis and related complications is still unclear. The present study aimed to determine the mechanisms of Malvidin's potential protection from lipopolysaccharide (LPS)-induced spleen injury model of sepsis. In the LPS-induced mouse spleen injury model of sepsis, pretreatment with Malvidin was performed to assess morphological damage in spleen tissue and to detect the expression of mRNA levels of serum necrosis factor α, interleukin 1ß and interleukin 6, and IL-10. Apoptosis was detected using the TUNEL technique, and the levels of oxidative stress-related oxidase and antioxidant enzymes were measured by kit to assess the effect of Malvidin on inflammation and oxidative stress associated with septic spleen injury. The results of this study indicated that Malvidin was be a potentially effective drug for the treatment of sepsis.

Indium selenide/silver phosphate hollow microsphere S-scheme heterojunctions for photocatalytic hydrogen production with simultaneous degradation of tetracycline.

Designing heterojunction photocatalysts with strong interfacial interactions is an effective way to reduce the recombination of photogenerated charge carriers. Here, silver phosphate (Ag3PO4) nanoparticles are coupled with hollow flower-like indium selenide (In2Se3) microspheres by a facile Ostwald ripening and in-situ growth method, resulting in the construction of In2Se3/Ag3PO4 hollow microsphere step-scheme (S-scheme) heterojunction with a large contact interface. The flower-like In2Se3 with hollow and porous structure provides a large specific surface area and numerous active sites for photocatalytic reactions to take place. The photocatalytic activity was tested by measuring the hydrogen evolution from antibiotic wastewater, and the H2 evolution rate of In2Se3/Ag3PO4 reached 4206.4 µmol g-1h-1 under visible light, which is approximately 2.8 times greater than that of In2Se3. In addition, the amount of tetracycline (TC) degradation when it was used as a sacrificial agent is about 54.4% after 1 h. On the one hand, Se-P chemical bonds act as electron transfer channels in the S-scheme heterojunctions, which can facilitate the migration and separation of photogenerated charge carriers. On the other hand, the S-scheme heterojunctions can retain the useful holes and electrons with higher redox capacities, which is very favorable for the generation of more •OH radicals and the photocatalytic activity is greatly enhanced. This work provides an alternative design approach for photocatalysts toward hydrogen evolution in antibiotic wastewater.

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Sepsis is a complex syndrome caused by multiple pathogens and involves multiple organ failure, particularly spleen dysfunction. In 2017, the worldwide incidence was 48.9 million sepsis cases and 11 million sepsis-related deaths were reported (Rudd et al., 2020). Inflammation, oxidative stress, and apoptosis are the most common pathologies seen in sepsis. Liensinine (LIE) is a bisbenzylisoquinoline-type alkaloid extracted from the seed embryo of Nelumbo nucifera. Lotus seed hearts have high content of LIE which mainly has antihypertensive and antiarrhythmic pharmacological effects. It can exert anti-carcinogenic activity by regulating cell, inflammation, and apoptosis signaling pathways (Manogaran et al., 2019). However, its protective effect from sepsis-induced spleen damage is unknown. In this research, we established a mouse sepsis model induced by lipopolysaccharide (LPS) and investigated the protective effects of LIE on sepsis spleen injury in terms of inflammatory response, oxidative stress, and apoptosis.

Photo Energy-Enhanced Oxygen Reduction and Evolution Kinetics in Zn-Air Batteries.

Harvesting solar energy directly to boost the sluggish kinetics of oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) on an air cathode is a promising approach. Herein, we synthesize a step-scheme (S-scheme) titanium dioxide-indium selenide (TiO2-In2Se3) heterojunction catalyst. The onset potential in ORR under light illumination reaches 1.28 V and the onset potential decreases to 0.48 V in OER. When an S-scheme TiO2-In2Se3 heterojunction is exposed to light, photogenerated electrons at the conduction band (CB) of TiO2 migrate to the valence band (VB) of In2Se3 due to the built-in electric field. The photogenerated electrons with strong reduction capability on the CB of In2Se3 and the holes with strong oxidation capability on the VB of TiO2 boost the cathode reaction kinetics (ORR/OER). The excellent outcome reveals tremendous commercial potential of photo-enhanced Zn-air batteries.

LncRNA DDX11-AS1 Promotes Chemoresistance through LIN28A-Mediated ATG12 mRNA Stabilization in Breast Cancer.

INTRODUCTION: During breast cancer chemotherapy, the chemoresistance that frequently accompanies the treatment has become a big challenge. Long noncoding RNAs (LncRNAs) have been related to the development of chemoresistance in multiple cancer types. LncRNA DDX11-AS1 has shown a carcinogenic role in lung and colorectal cancer and was reported to enhance oxaliplatin resistance in gastric cancer and Taxol insensitivity in esophageal cancer. But its role in breast cancer chemotherapy drug resistance remains unknown. This study aimed to investigate the function and mechanism of lncRNA DDX11-AS1 in breast cancer chemoresistance. METHODS: The relationship between DDX11-AS1 and adriamycin (ADR) resistance was confirmed by qPCR, cell viability tests, and survival analysis. Then, RNA immunoprecipitation was conducted to evaluate the interaction between DDX11-AS1 and RNA-binding protein LIN28A. The regulation effect of LIN28A on autophagy-related genes ATG7 or ATG12 was detected by RNA stability assay and Western blot. Their correlation analysis was evaluated in GEO datasets and further validated by immunohistochemical results. The clinical significance of DDX11-AS1, ATG7, or ATG12 was evaluated by Kaplan-Meier Plotter analysis. RESULTS: Here, we reported DDX11-AS1 was significantly upregulated in chemoresistant breast cancer cells and overexpression of DDX11-AS1 promoted ADR resistance in breast cancer. LIN28A could interact with DDX11-AS1 and was involved in DDX11-AS1-mediated ADR resistance. Interfering with LIN28A reversed DDX11-AS1-induced ADR resistance. LIN28A could increase the protein level of ATG7 and ATG12 by increasing their mRNA stability. Survival analysis showed that ATG12 expression level was negatively correlated with the prognosis of breast cancer patients. CONCLUSION: This study clarifies the role of DDX11-AS1 in breast cancer chemoresistance and revealed a new mechanism, that is, interacting with LIN28A to stabilize ATG7 and ATG12 and jointly promote chemorefractory. These findings warrant further in vivo investigations to study DDX11-AS1 as a potential target to overcome chemoresistance.

A dual S-scheme TiO2@In2Se3@Ag3PO4 heterojunction for efficient photocatalytic CO2 reduction.

The excellent photoresponse of semiconductors enables them to be promising photocatalysts for CO2 reduction, but practical application is hampered by fast recombination of photogenerated carriers, low CO2 capture capacity and poor stability. Herein, mesoporous hollow nanospheres of a dual S-scheme titanium dioxide@indium selenide@silver phosphate (TiO2@In2Se3@Ag3PO4) heterojunction with a large specific surface area are designed and synthesized. The products of photocatalytic CO2 reduction are CH4, CH3OH and CO with yields of 3.98, 4.32 and 8.2 µmol g-1 h-1, respectively, and the photocatalysts exhibit excellent cycle performance. The excellent photocatalytic performance is attributed to the large specific surface area of the samples and the construction of dual S-scheme heterojunctions. The large specific surface area can provide sufficient active sites for photocatalytic activity. Simultaneously, the built-in electric field (IEF) in the dual S-scheme exposed to light can facilitate the migration of photogenerated electrons from the CB of the oxidation photocatalyst (OP) to the VB of the reduction semiconductor (RP), where they recombine with the photogenerated holes on the VB of the RP, leaving behind photogenerated carriers with high redox ability for photocatalytic activity. This work provides new insights into the mechanism and design of highly efficient heterojunction photocatalysts for CO2 reduction.

Malvidin protects against lipopolysaccharide-induced acute liver injury in mice via regulating Nrf2 and NLRP3 pathways and suppressing apoptosis and autophagy.

Sepsis-related acute liver injury (ALI) is a fatal disease associated with many complications. Recent studies indicate that malvidin, an active flavonoid, has multiple bioactivities including anti-oxidant and anti-inflammation. However, the protective roles of malvidin against LPS-induced ALI are unknown. The purpose of this research is to explore whether malvidin has biological activities on LPS-induced ALI in mice and the underlying mechanisms. Male C57 mice were injected intraperitoneally with malvidin for five days and the mice were euthanized 6 h after LPS (10 mg/kg body weight) intraperitoneal injection. Multiple methods of H&E staining, biochemical kits, qRT-PCR assay, western blotting analysis, TUNEL and transmission electron microscope (TEM) were used. Results showed that decreased ALT, AST levels and alleviated histopathological damage of liver tissue were observed in malvidin pretreatment group in mice. Then, malvidin prevented LPS-induced reduction of antioxidant enzyme activities such as superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase (CAT) via up-regulating nuclear factor E2-related factor2 (Nrf2) pathway. In addition, in malvidin pretreatment groups, mRNA levels of pro-inflammatory cytokines (TNF-α，IL-1ß, IL-6) and protein levels of NOD-like receptor protein 3 (NLRP3) inflammasome in the liver were significantly down-regulated. We also found that the malvidin could reduce the expression of apoptosis key protein and TUNEL-labeled apoptotic hepatocytes. Furthermore, malvidin inhibited the protein expression of ATG5, p62 and the ratio of LC3-II/LC3-I. In conclusion, our study firstly suggests that malvidin is a potentially protective agent against LPS-induced ALI through up-regulating Nrf2 signaling pathway, suppressing NLRP3 inflammasome and inhibiting apoptosis and autophagy.

Changes in chemical components and antitumor activity during the heating process of Fructus Arctii.

Context: The dried fruits of Arctium lappa L. have been used in two forms in traditional Chinese medicine; crude and stir-heating Fructus Arctii. However, its processed product possesses better activity. Objective: In this study, the chemical constituents of both crude and processed Fructus Arctii and their antiproliferative activities were evaluated. Materials and methods: The seven main active components in crude and various processed Fructus Arctii were quantitatively determined using high-performance liquid chromatography (HPLC). According to the actual amount in crude and five processed samples, seven single components were combined as multi-component combinations with six different proportions. The antiproliferative activities of these compatibility component groups were examined using the CCK-8 assay. Results: During the heating process, the proportion of the seven main components changed dynamically. The contents of 3-caffeoylquinic acid (3-CQA), 3,5-dicaffeoylquinic acid (3,5-diCQA), and arctiin (ARC) declined, while the contents of 4-caffeoylquinic acid (4-CQA), 3,4-dicaffeoylquinic acid (3,4-diCQA), 4,5-dicaffeoylquinic acid (4,5-diCQA), and arctigenin (ARG) increased very significantly. Discussion and conclusions: The results also indicated that seven components in the processed samples had higher cytotoxic profiles against HL-60 cells than those in the crude sample. Therefore, the heating process may enhance the antitumor activity of Fructus Arctii by changing the proportion of active components.

Pudilan xiaoyan oral liquid alleviates LPS-induced respiratory injury through decreasing nitroxidative stress and blocking TLR4 activation along with NF-ΚB phosphorylation in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Pudilan xiaoyan oral liquid (PDL), collected in Chinese Pharmacopoeia, has been used clinically for treating inflammatory diseases such as upper respiratory tract infection diseases. However, its potential anti-inflammation and the mechanism are still unclear. MATERIALS AND METHODS: lipopolysaccharide (LPS) was used to induce respiratory inflammation of mice by intratracheal administration. UPLC/MS was performed for components analysis of PDL. Enzyme-linked immune sorbent assay (ELISA) was conducted for determining interleukin-6(IL-6), interleukin-1ß(IL-1ß) and tumor necrosis factor-α(TNF-α) in serum and supernatant of tracheal tissue while Nitric oxide assay kit for nitric oxide (NO) content. Hematoxylin-Eosin (HE) staining was applied to evaluate pathological lesions. Western blotting analysis (WB) and Immunohistochemistry(IHC) were employed for the determination of Toll-like receptors 4(TLR4), TNF-α, IL-6, inducible nitric oxide synthase(iNOS) and nuclear factor-kappa B p65 (NF-κB p65) protein expressions. RESULTS: Seven major compounds of PDL were analyzed simultaneously. The treatment of PDL could attenuate LPS-induced histopathological damage of tracheal tissues, followed by reducing pro-inflammation mediators including TNF-α and IL-6 in serum and supernatant of tracheal tissue. LPS-induced nitroxidative stress including NO content and iNOS expression was inhibited significantly by PDL. Furthermore, PDL also down-regulated NF-kB p65 phosphorylation and TLR4 expressions. CONCLUSION: The results indicated that the PDL had a protective effect on LPS-induced respiratory inflammation injury in mice. Our findings for the first time provide experimental evidence for the application of PDL on respiratory inflammation injury in clinical practice.