Effects of crayfish shell powder and bamboo-derived biochar on nitrogen conversion, bacterial community and nitrogen functional genes during pig manure composting.

This study investigated the effects of crayfish shell powder (CSP) and bamboo-derived biochar (BDB) on nitrogen metabolism, bacterial community and nitrogen functional genes during pig manure composting. Four treatments were established: CP (with no additives), TP1 (5 % BDB), TP2 (5 % CSP) and TP3 (2.5 % BDB + 2.5 % CSP). Compared to CP, the germination index (GI) of TP reached > 85 % 10 days earlier. Meanwhile, TP3 reduced NH3 and N2O emissions by 42.90 % and 65.9 %, respectively, while increased TN (total nitrogen) concentration by 5.43 g/kg. Furthermore, additives changed the bacterial structure and formed a beneficial symbiotic relationship with essential N-preserving bacteria, thereby enhancing nitrogen retention throughout the composting process. Metagenomic analysis revealed that additives upregulated nitrification genes and downregulated denitrification and nitrate reduction genes, ultimately improving nitrogen cycling and mitigating NH3 and N2O emissions. In conclusion, the results confirmed that TP3 was the most effective treatment in reducing nitrogen loss.

Sulfonate Derivatives Containing a Kakuol Moiety as Potential Fungicidal Candidates: Design, Synthesis and Antifungal Activity Evaluation.

As a part of our continuing exploration to discover new potential promising fungicide candidates, eighteen sulfonate derivatives (3a-3r) containing a kakuol moiety were designed and synthesized. Synthetic sulfonate derivatives were tested comprehensively for antifungal activities against four plant pathogenic fungi (Botrytis (B.) cinerea, Valsa (V.) mali, Fusarium (F.) graminearum, Sclerotinia (S.) sclerotiorum), and their structure activity relationships were summarized. Especially, derivatives 3i and 3j exhibited remarkable activity against V. mali, with the inhibition rates of 99.8 and 100%, which were slightly superior to that of carbendazim (98.9%), a reference fungicide. Moreover, derivatives 3a, 3k and 3q possess the broader antifungal spectrum against three tested plant pathogenic fungi with inhibition rates over 60%. Structure-activity relationship (SAR) analysis indicated that the introduction of 2-F or 3-F into the benzene ring would give rise to a remarkable increase of the antifungal activity against V. mali.

A novel tetranuclear Cu(ii) complex for DNA-binding and in vitro anticancer activity.

A novel tetranuclear Cu(ii) complex (TNC) was successfully synthesized and characterized by X-ray single crystal diffraction. The interaction of the complex with calf thymus DNA (CT-DNA) has been studied by UV-vis absorption titration, fluorescence technology and molecular docking. The results indicated that TNC could bind to the DNA through an intercalative mode. The agarose gel electrophoresis experiment showed that TNC could cleave supercoiled plasmid DNA into linear DNA. The anticancer activity of TNC was tested on four cancer cell lines: MCF7, A549, 4T1 and HepG2. The results indicated that TNC shown significant activity against all of above cell lines.

Co-delivery of docetaxel and p53 gene from cationic nanoparticles based on poly (l-lactide) and low-molecular-weight polyethyleneimine (PEA).

Recent findings revealed that low-concentration paclitaxel(DTX) could enhance cytotoxicity by upregulating p53 expression in lung cancer cell lines. So, co-delivery of DTX and RFP-p53 gene with PEA nanoparticles (NPs) was studied. The prepared DTX loaded PEA NPs (PEA/DTX) were characterized by particle size distribution, morphology, zeta potential, and crystallography and cytotoxicity. Results showed that the PEA/DTX NPs had a mall particle size (≤100 nm), moderate zeta potential (≥40 mV) and drug loading of 9.0%, DTX was released from PEA/DTX NPs in an extended period in vitro. More important, agarose gel electrophoresis showed that PEA/DTX cationic NPs were able to completely bind RFP-p53 gene with mean particles size and zeta potential. Studies on cellular uptake of (PEA/DTX)/RFP-p53 NPs demonstrated that both drug and gene were effectively taken up by A549 tumor cells. It was found that intravenous injection of (PEA/DTX)/RFP-p53 NPs efficiently inhibited growth of subcutaneous A549 carcinoma in vivo (p < 0.05) and was significantly less side effect than that of mice treated with the other groups. Therefore, the (PEA/DTX)/RFP-p53 NPs might be a promising candidate for A549 cancer therapy.

Simultaneous self-supply of H2O2 and GSH-depleted intracellular oxidative stress for enhanced photodynamic/photothermal/chemodynamic therapy.

Herein, we designed a new nanoplatform for combined PDT/PTT/CDT through simultaneously self-supplying H2O2 and depleting GSH using one single laser irradiation. The nanoplatform was capable of generating multiple reactive oxygen species (ROS), such as 1O2, O2-˙ and ˙OH, resulting in cell death. Moreover, the nanoplatform demonstrated low dark toxicity, high phototoxicity and better biosafety. In vivo animal experiments showed that the tumor growth was efficiently inhibited.

Monolayer-Graphene-Based Tunable Absorber in the Near-Infrared.

In this paper, a tunable absorber composed of asymmetric grating based on a graphene-dielectric-metal structure is proposed. The absorption of the absorber can be modified from 99.99% to 61.73% in the near-infrared by varying the Fermi energy of graphene, and the absorption wavelength can be tuned by varying the grating period. Furthermore, the influence of other geometrical parameters, the incident angle, and polarization are analyzed in detail by a finite-difference time-domain simulation. The graphene absorbers proposed in this paper have potential applications in the fields of stealth, sense, and photoelectric conversion. When the absorber that we propose is used as a gas sensor, the sensitivity of 200 nm/RIU with FOM can reach up to 159 RIU-1.

Omnidirectional and compact transmissive chromatic polarizers based on a dielectric-metal-dielectric structure.

High-performance omnidirectional transmissive chromatic polarizers based on a one-dimensional dielectric-metal-dielectric subwavelength grating structure are proposed. The incident angle-insensitive properties, azimuthal angle-insensitive properties and polarization features are investigated thoroughly to realize the proposed omnidirectional transmissive chromatic polarizers. The color difference at different angles for the proposed yellow polarizers is less than 0.9746, and the extinction ratio at different angles for the proposed cyan polarizers exceeds 26. Analysis of the power density profiles for the transverse electric (TE) and transverse magnetic (TM) polarizations show that surface plasmon resonance and high refractive index contrast properties lead to excellent polarization features and high angular tolerance.

A simultaneously GSH-depleted bimetallic Cu(ii) complex for enhanced chemodynamic cancer therapy.

A bimetallic Cu(ii) complex as a novel antitumor chemodynamic therapy agent with glutathione (GSH) depletion properties is successfully synthesized and well characterized. In tumor cells, the Cu2+ ions of the complex are reduced to Cu+ ions by GSH and then catalyzed by the overexpressed H2O2 to generate highly cytotoxic hydroxyl radicals (˙OH) that kill cancer cells. The complex is quickly taken up by cancer cells and distributed in multiple organelles including mitochondria and the nucleus. The complex demonstrates good cytotoxicity toward various cancer cell lines. However, its toxicity toward normal cells is significantly lower than that toward cancer cells due to the limited expression of H2O2. In addition, the complex could arrest the cell cycle of the G0/G1 phase, thereby inducing apoptosis rather than necrosis.

A novel Mn-Cu bimetallic complex for enhanced chemodynamic therapy with simultaneous glutathione depletion.

A bimetallic complex, containing Mn(ii) and Cu(ii) moieties, was synthesized for chemodynamic therapy (CDT) of cancer. The complex was capable of generating a hydroxyl radical (˙OH) via a Fenton-like reaction involving a Mn complex, and simultaneously depleting glutathione via a Cu complex induced oxidative reaction, thereby enhancing the efficiency of CDT.

Complement depletion with cobra venom factor alleviates acute hepatic injury induced by ischemia­reperfusion.

Increasing evidence has demonstrated that complement activation is required for ischemia­reperfusion injury (IRI)­induced hepatic damage, and cobra venom factor (CVF) can deplete the complement components. The aim of the current study was to investigate the effect and intrinsic mechanism of CVF pretreatment on IRI­induced acute hepatic injury in rats. Acute hepatic injury in rats was induced by bone fracture to simulate trauma, followed by hemorrhage for 90 min, and then the rats were resuscitated for a period of 20 min of reperfusion. The survival times under different CVF treatment doses and schedules for rats with IRI were evaluated. Hepatic tissues and serum samples were analyzed for acute hepatic injury, complement activation, inflammatory mediator release and apoptosis at predetermined times and compared between the IRI group and the CVF pretreatment + IRI groups. Compared to the rats with IRI alone, the survival times were significantly improved among rats with IRI receiving a high­dose or low­dose CVF pretreatment (all P<0.01). Upon histological examination, severe hepatic damage was observed in the rats with IRI, accompanied by liver function deterioration, complement and membrane attack complex activation, inflammatory mediator release and hepatic cell apoptosis. CVF pretreatment significantly attenuated the hepatic injury through depletion of anaphylatoxic C5a and membrane attack complex C5b­9 activation, and subsequent inhibition of inflammatory mediator release and hepatic cell apoptosis (all P<0.05). The results indicated that CVF pretreatment ameliorates IRI­induced acute hepatic injury. However, further studies are required to determine whether this therapy could be a potential agent for the treatment of IRI injuries in clinical settings.

Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation.

Silybin is one of the main flavonoids produced by milk thistle, which has been used in the treatment of liver diseases. In this study, we examined the protective effects and possible mechanisms of action of silybin in lipopolysaccharide (LPS)­induced lung injury and inflammation. Pre-treatment of mice with silybin significantly inhibited LPS-induced airway inflammatory cell recruitment, including macrophages, T cells and neutrophils. The production of cytokines, such as interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in bronchoalveolar fluid and serum was also decreased following treatment with silybin. Elevated cytokine mRNA levels induced by LPS in lung tissue were all suppressed by silybin and lung histological alterations were also improved. In addition, experiments using cells indicated that silybin significantly decreased the mRNA levels and secretion of IL-1ß and TNF-α in THP-1 cells. Moreover, the mechanisms responsible for these effects were attributed to the inhibitory effect of silybin on nuclear factor-κB (NF-κB) signaling and NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. The data form our study thus support the utility of silybin as a potential medicine for the treatment of acute lung injury­associated inflammation and pathological changes. Silybin exerts protective effects against lung injury by regulating NF-κB signaling and the NLRP3 inflammasome activation.

[Acuuncture combined with swallowing training for post-stroke dysphagia: a randomized controlled trial].

OBJECTIVE: To observe the clinical efficacy of deep acupuncture at Lianquan (CV 23) and Yifeng (TE 17) combined with swallowing training for post-stroke dysphagia. METHODS: Sixty cases of post-stroke dys phagia were randomly divided into an observation group and a control group, 30 cases in each one. Patients in the observation group, based on the regular acupuncture treatment, were treated with deep acupuncture at Lianquan (CV 23) and Yifeng (TE 17), once a day, 30 min per treatment; also swallowing training was combined, twice a day, 20 min per treatment. Patients in the control group were treated with swallowing training. All the patients were treated with regular treatment of stroke. Six days of treatment were taken as one session, and totally 3 sessions were given with an interval of one day between sessions. The video fluoroscopic swallowing study (VFSS) dysphagia evaluation scale and Watian water swallow test (WWST) were evaluated before and after treatment also the clinical efficacy and the recovery time of two groups were compared. RESULTS: After treatment, the VFSS score in the observation group was significantly superior to that in the control group (P < 0.01); the WWST in the observation group was significantly superior to that in the control group (P < 0.01). The cured rate was 70.0% (21/30) in the observation group, which was significantly superior to 43.3% (13/30) in the control group (P < 0.01); the total effective rate was 86.7% (26/30) in the observation group, which was significantly superior to 66.7% (20/30) in the control group (both P < 0.01). The clinical recovery time in the observation group was significantly shorter than that in the control group (P < 0.01). CONCLUSION: Deep acupuncture at Lianquan (CV 23) and Yifeng (TE 17) combined with swallowing training could effectively improve post-stroke swallow function.

Decreased Histone Deacetylase 2 (HDAC2) in Peripheral Blood Monocytes (PBMCs) of COPD Patients.

BACKGROUND: Histone deacetylase 2 (HDAC2) is a class I histone deacetylase family member that plays a critical role in suppressing inflammatory gene expression in the airways, lung parenchyma, and alveolar macrophages in patients with chronic obstructive pulmonary disease (COPD). However, the expression of HDAC2 in peripheral blood monocytes (PBMCs), nuclear factor kappa B (NF-κB) p65, and serum inflammatory cytokine levels in COPD patients, smokers, and non-smokers remains unclear. METHODS: PBMCs were obtained from COPD patients, healthy smokers, and healthy nonsmokers. The HDAC2 and NF-κB p65 expression were quantified by Western Blot. HDAC activity was assessed by an HDAC fluorometric immunoprecipitation activity assay kit. Serum tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8) levels were measured by ELISA. RESULTS: HDAC2 expression and HDAC activity were decreased in PBMCs in COPD patients compared with smokers and non-smokers. Increased NF-κB p65 expression, serum TNF-α and IL-8 levels were observed in COPD patients compared with nonsmokers. The FEV1%pred was positively correlated with HDAC2 expression and HDAC activity in COPD patients. Smokers had decreased HDAC activity, increased NF-κB p65 expression and serum TNF-α compared with nonsmokers. CONCLUSIONS: HDAC2 expression was decreased in PBMCs of COPD patients and was correlated with disease severity. The reduction of HDAC2 expression not only directly enhances the expression of inflammatory genes, but may account for the activation of NF-κB mediated inflammation. Decreased HDAC2 may serve as a potential biomarker of COPD and predict the decline of lung function.

[Comparison of clinical efficacy between continuous renal replacement therapy and intermittent haemodialysis for the treatment of sepsis-induced acute kidney injury].

Objective: To compare the clinical effects between continuous renal replacement therapy (CRRT) and intermittent haemodialysis (IHD) for the treatment of sepsis-induced acute kidney injury (AKI). Methods: A prospective study was conducted. Seventy-three patients with sepsis-induced AKI admitted to the intensive care units (ICUs) of Tianjin Hospital and Tianjin First Center Hospital from January to December in 2014 were enrolled. They were randomly divided into two groups: CRRT group (n = 35) and IHD group (n = 38). Data were recorded for the patients in two groups before treatment, including acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score, mean arterial pressure (MAP), urine volume, and the levels of C-reactive protein (CRP) and serum creatinine (SCr) before and 1 week after treatment, the time of recovery of urine volume, the length of ICU stay, the duration of organ support, and the incidence of cardiovascular events. Results: There was no statistically significant difference in APACHE Ⅱ scores (21.63±2.46 vs. 21.34±2.46), MAP [mmHg (1 mmHg = 0.133 kPa): 71.26±10.70 vs. 75.74±15.17], urine volume (mL: 404.00±79.13 vs. 438.97±87.17), CRP (mg/L: 100.94±14.73 vs. 95.17±27.03), and SCr (µmol/L: 394.02± 50.26 vs. 390.47±54.42) before treatment between CRRT group and IHD group (all P > 0.05). One week after treatment, compared to the IHD group, CRRT could dramatically reduce the levels of CRP (mg/L: 41.05±10.15 vs. 60.21±14.78, t = 6.401, P < 0.001), SCr (µmol/L: 185.97±65.48 vs. 232.02±71.93, t = 2.862, P = 0.006), urine output recovery time (days: 7.94±3.06 vs. 11.08±3.71, t = 3.923, P < 0.001), the length of ICU stay (days: 9.54±3.39 vs. 13.42±3.89, t = 4.521, P < 0.001), organ support time (days: 3.23±2.70 vs. 6.34±3.36, t = 4.343, P < 0.001), and the incidence of cardiovascular events [23.53% (8/35) vs. 39.47% (15/38), χ2 = 5.509, P = 0.025]. Conclusion: Compared to IHD, CRRT can more efficiently help patients with sepsis-induced AKI in removing excessive water, metabolic waste, and lower the levels of pro-inflammatory cytokines, maintain homeostasis of the internal environment, lower the adverse effects on cardiovascular system, so that it significantly improve the prognosis of patients, shorten the time of organ support and the length of ICU stay.

[Effect of WS070117M1 on chronic obstructive pulmonary disease in mice and the underling mechanisms of anti-inflammation].

The aim of this study is to investigate the anti-inflammatory effect of the adenosine derivative N6-(3-hydroxylaniline) adenosine (WS070117M1) on cigarette smoke plus LPS (lipopolysaccharide)-induced chronic obstructive pulmonary disease (COPD) in mice and its mechanism. COPD model was established by exposing male BALB/c mice to cigarette smoke and challenged with LPS inhalation. Supernatants of bronchoalveolar lavage fluid (BALF) were harvested and IL-1ß, IL-6, IL-8 and TGF-ß1 levels were measured by ELISA (enzyme-linked immunesorbent assay). The number of total white blood cells and neutrophils in bronchoalveolar lavage fluid was counted separately. Lung tissue was stained with Mayer 's hematoxylin and eosin for histopathologic examination. pAMPKa protein expression and distribution of lung tissue were analyzed by immunohistochemistry method. In vitro, levels of AMPKα phosphorylation in phorbol-12- myristate-13-acetate (PMA) differentiated THP-1 cells was detected by immunohistochemistry, IL-8 level in supernatants of cigarette smoke condensate stimulating PMA differentiated THP-1 cells was measured by ELISA. The results showed that WS070117M1 treatment significantly activated AMPKa in the lung tissue. It also resulted in down regulation of IL-1ß, IL-6, IL-8 and TGF-ß1 levels in bronchoalveolar lavage fluid and IL-8 level in cigarette smoke condensate stimulating PMA differentiated THP-1 cells. In addition, WS070117M1 could inhibit the recruitment of total white blood cells and neutrophils. These results suggest that WS070117M1 may alleviate the airway inflammation by activating AMPK in the lung tissue.

Epigallocatechin-3-Gallate (EGCG) Attenuates Traumatic Brain Injury by Inhibition of Edema Formation and Oxidative Stress.

Traumatic brain injury (TBI) is a major cause of mortality and long-term disability, which can decrease quality of life. In spite of numerous studies suggesting that Epigallocatechin-3-gallate (EGCG) has been used as a therapeutic agent for a broad range of disorders, the effect of EGCG on TBI remains unknown. In this study, a weight drop model was established to evaluate the therapeutic potential of EGCG on TBI. Rats were administered with 100 mg/kg EGCG or PBS intraperitoneally. At different times following trauma, rats were sacrificed for analysis. It was found that EGCG (100 mg/kg, i.p.) treatment significantly reduced brain water content and vascular permeability at 12, 24, 48, 72 hour after TBI. Real-time PCR results revealed that EGCG inhibited TBI-induced IL-1ß and TNF-α mRNA expression. Importantly, CD68 mRNA expression decreasing in the brain suggested that EGCG inhibited microglia activation. Western blotting and immunohistochemistry results showed that administering of EGCG significantly inhibited the levels of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) expression. TBI-induced oxidative stress was remarkably impaired by EGCG treatment, which elevated the activities of SOD and GSH-PX. Conversely, EGCG significantly reduced the contents of MDA after TBI. In addition, EGCG decreased TBI-induced NADPH oxidase activation through inhibition of p47(phox) translocation from cytoplasm to plasma membrane. These data demonstrate that EGCG treatment may be an effective therapeutic strategy for TBI and the underlying mechanism involves inhibition of oxidative stress.

[A study of apoptosis of murine platelet induced by lipopolysaccharide derived from Escherichia coli in vitro].

OBJECTIVE: To observe whether lipopolysaccharide ( LPS ) derived from Escherichia coli ( E.coli ) can induce apoptosis of murine platelets in vitro. METHODS: Washed platelet suspension was prepared and adjusted to the final concentration of 3×10(8)/mL. According to the difference in stimulants, samples were divided into control group ( non-calcium Tyrode buffer ), thrombin-treated group ( 1 U/mL final concentration and non-calcium TB ) and LPS in different concentrations treated groups ( 1, 10 and 100 µg/mL final concentration respectively and non-calcium TB ). To each specimental group corresponding stimulus was added and incubated 30 minutes at room temperature. Chemiluminescence was adopted to determine the concentration of adenosine triphosphate ( ATP ) and the activity of cysteinyl aspartate specific proteinase-3 ( caspase-3 ). The percentage of Annexin V positive platelets was determined by flow cytometry to reflect the level of phosphatidylserine ( PS ) exposure. Mean channel fluorescence ( MCF ) of platelets was determined by flow cytometry for reflecting the level of mitochondrial inner transmembrane potential (Δψm ) depolarization. RESULTS: Compared with control group, the ATP concentration in thrombin-treated group was decreased obviously [ relative light unit ( RLU ): ( 5.46±0.14 )×10(5) vs. ( 6.25±0.26 )×10(5), P < 0.05 ], Annexin V positive ratio [ ( 50.43±2.45 )% vs. ( 1.58±0.25 )%, P < 0.05 ] and caspase-3 activity [ RLU: ( 26.92±1.60 )×10(3) vs. ( 1.30±0.10 )×10(3), P < 0.05 ] were increased obviously, and platelets MCF was lowered significantly [ ( 8.32±0.58 )×10(4) vs. ( 13.05±1.10 )×10(4), P < 0.05 ], suggesting an increase in Δ ψm depolarization. After being treated with different concentrations of LPS, ATP concentration, Annexin V positive ratio and caspase-3 activity were increased obviously, platelet MCF was decreased obviously, suggesting Δψm depolarization was increased in a concentration-dependent manner. Compared with control group, 1 µg/mL LPS could increase Annexin V positive ratio [ ( 10.45±1.08 )% vs. ( 1.58±0.25 )%, P < 0.05 ], elevate caspase-3 activity [ RLU: ( 14.06±0.61 )×10(3) vs. ( 1.30±0.10 )×10(3), P < 0.05 ], and decrease MCF significantly [ ( 9.48±0.50 )×10(4) vs. ( 13.05±1.10 )×10(4), P < 0.05 ]. The ATP concentration, Annexin V positive ratio and caspase-3 activity reached maximum levels after the treatment with 100 µg/mL LPS, and they were higher obviously than those of the control group [ ATP ( RLU ): ( 7.00±0.03 )×10(5) vs. ( 6.25±0.26 )×10(5), Annexin V positive ratio: ( 55.35±2.42 )% vs. ( 1.58±0.25 )%, casepase-3 ( RLU ): ( 32.00±3.75 )×10(3) vs. ( 1.30±0.10 )×10(3), all P < 0.05 ], and platelets MCF reached trough levels, and they were obviously lower than those of the control group [ ( 4.69±0.55 )×10(4) vs. ( 13.05±1.10 )×10(4), P < 0.05 ]. CONCLUSIONS: E.coli LPS can induce an increase in ATP, PS exposure, Δψm depolarization and activity increase of caspase-3 on mouse platelet in vitro, which indicate that LPS can induce apoptosis of platelets in a concentration-dependent manner.

FLLL31, a derivative of curcumin, attenuates airway inflammation in a multi-allergen challenged mouse model.

Signal transducer and activator of transcription protein 3 (STAT3), one of the major regulators of inflammation, plays multiple roles in cellular transcription, differentiation, proliferation, and survival in human diseases. Dysregulation of STAT3 is related to the severe airway inflammation associated with asthma. FLLL31 is a newly developed compound based on the herbal medicine curcumin, which specifically suppresses the activation of STAT3. However, the function of FLLL31 on inflammatory diseases, especially on the regulation of airway inflammation, has not been fully studied. In our prior investigations, we developed a mouse model that was challenged with a mixture of DRA allergens (including house dust mite, ragweed, and Aspergillums species) to mimic the severe airway inflammation observed in human patients. In this study, we performed a series of experiments on the inflammatory regulation activities of FLLL31 in both in vitro cultured cells and our in vivo DRA-challenged mouse model. Our results show that FLLL31 exhibits anti-inflammatory effects on macrophage activation, lymphocyte differentiation, and pro-inflammatory factor production. Importantly, FLLL31 significantly inhibited airway inflammation and recruitment of inflammatory cells in the DRA-challenged mouse model. Based on these results, we conclude that FLLL31 is a potential therapeutic agent that can be used against severe airway inflammation diseases.

[Advance in the research on P2X7 and inflammatory respiratory diseases].

P2X7 is the most important subtype of the ATP receptors known so far. Recent investigations showed that the downstream signaling pathway of P2X7 is coupled with several key inflammatory molecules including IL-1beta and IL-18, this suggests P2X7 might have roles in the inflammatory diseases. Moreover, attenuation of P2X7 by selective antagonists in vitro and knockout mice in vivo reducing the inflammatory response indicated that P2X7 is a potential therapeutic target for inflammatory diseases. However, most previous studies on P2X7 were focused on nerve system diseases most, while its effects in inflammatory respiratory diseases, especially in asthma, chronic obstructive pulmonary disease (COPD) and lung cancer have been poorly investigated. In this paper, we reviewed the research progress on the structure, distribution, biological activities of P2X7 and its relationship with inflammatory respiratory diseases including asthma, COPD and lung cancer, along with the development of P2X7 antagonist as therapeutics.