The effect of intravenous lidocaine on postoperative cognitive dysfunction: a systematic review and meta-analysis.

BACKGROUND: Postoperative cognitive dysfunction (POCD) has been reported as a significant complication in elderly patients. Various methods have been proposed for reducing the incidence and severity of POCD. Intravenous lidocaine administration has been reported in the literature to reduce POCD, but the effect of lidocaine remains controversial. METHODS: We screened Medline, Embase, Cochrane Library, and China National Knowledge Infrastructure (up to April 2022) databases following a search strategy for intravenous lidocaine on POCD. We also screened related bibliographies on lidocaine for POCD. Ten articles comprising 1517 patients were selected and analyzed. We divided the postoperative follow-up period as follows: short term (<30 days), medium term (30-90 days), and long term (>90 days). OUTCOMES: We found that lidocaine could attenuate the overall incidence of POCD, especially in the short term. There were no differences between lidocaine and placebo on the overall severity of POCD. CONCLUSION: Lidocaine administered intravenously could attenuate the overall incidence of POCD and its severity in the short term.

Heat-Stimuli Shape Memory Effect of Poly (ε-Caprolactone)-Cellulose Acetate Composite Tubular Scaffolds.

Small-diameter artery disease is the most common clinical occurrence, necessitating the development of small-diameter artificial blood vessels. In this study, seven types of poly(-caprolactone)-cellulose acetate (PCL-CA) composite nanofiber membranes were prepared with different proportions of PCL and CA. The adhesion and growth of Mc3t3-e1 cells were considered to confirm the in vitro cytocompatibility of PCL-CA membranes. A smooth stainless-steel mandrel with a diameter of 4 mm was used to roll up the prepared nanofiber membranes to produce the tubular scaffold with 50 °C hot water. The tubular scaffolds were subjected to axial and circumferential tensile tests. The mechanical performance of the PCL-CA tubular scaffold could be improved by increasing the layers. In addition, the burst pressure (BP) of the tubular scaffolds was increased with the layers, and the BPs of six-layer (2380 ± 36.8 mmHg) and eight-layer (3720 ± 80.5 mmHg) tubular scaffolds were much higher than that of the human saphenous vein (2000 mmHg). The compression shape memory performances of the PCL-CA tubular scaffold with different layers were also investigated to simulate and analyze the contraction and expansion of tubular scaffolds. The experimental results showed that the compression strain of the tubular scaffold in the diameter direction reached 35%, and the ultimate shape recovery rate reached 87%. However, the shape fixity rate and shape recovery rate increased, demonstrating that the optimum number of layers can improve the compression shape memory performance of the tubular scaffold. The results of this study, including comprehensive morphological and mechanical properties and cytocompatibility, indicated the potential applicability of PCL-CA tubular scaffolds as tissue engineering grafts.

Edaravone alleviated propofol-induced neural injury in developing rats by BDNF/TrkB pathway.

As a variety of free radical scavenger, edaravone has shown its potential in producing antioxidant, anti-inflammatory and neuroprotective effects in various disease models. However, the underlying mechanism behind the neuroprotective effects of edaravone remained unclear. This study is aimed at determining the effects of edaravone on neuroprotection and anti-inflammatory through a propofol-induced neural injury rat model. Firstly, an observation was made of apoptosis and neuroinflammation in the hippocampus of developing under the influence of propofol. It was found out that propofol could produce inflammatory effects in the hippocampus by enhancing the astrogliosis (GFAP) activation and elevating the level of neuronal nitric oxide synthase (nNOS), pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α). Meanwhile, the increase of apoptosis cells and the decrease of neurons (NeuN) were speculated to aggravate neural injury. Furthermore, it was demonstrated that edaravone intervention can reverse the neural apoptosis and inflammation. Additionally, the intraperitoneal injection of edaravone, the intraperitoneal injection of the brain-derived neurotrophic factor (BDNF)-mimicking small compound (7,8 dihydroxyflavone) and the intracranial injection of the exogenous BDNF were all respectively effective in alleviating the propofol-induced neural apoptosis and inflammation in the hippocampus. It was also found out that edaravone-activated downstream signalling through tyrosine kinase receptor B (TrkB) receptors in astrocyte, microglia and neuron. However, the neural injury of propofol had no impact on long-term learning and memory, except causing a short-term neurotoxicity. In conclusion, edaravone could alleviate the propofol-induced neural injury in developing rats through BDNF/TrkB pathway.

SHP2 inhibitor PHPS1 ameliorates acute kidney injury by Erk1/2-STAT3 signaling in a combined murine hemorrhage followed by septic challenge model.

BACKGROUND: Hypovolemic shock and septic challenge are two major causes of acute kidney injury (AKI) in the clinic setting. Src homology 2 domain-containing phosphatase 2 (SHP2) is one of the major protein phosphatase tyrosine phosphatase (PTPs), which play a significant role in maintaining immunological homeostasis by regulating many facets of immune cell signaling. In this study, we explored whether SHP2 signaling contributed to development of AKI sequential hemorrhage (Hem) and cecal ligation and puncture (CLP) and whether inactivation of SHP2 through administration of its selective inhibitor, phenylhydrazonopyrazolone sulfonate 1 (PHPS1), attenuated this injury. METHODS: Male C57BL/6 mice were subjected to Hem (a "priming" insult) followed by CLP or sham-Hem plus sham-CLP (S/S) as controls. Samples of blood and kidney were harvested at 24 h post CLP. The expression of neutrophil gelatinase-associated lipocalin (NGAL), high mobility group box 1 (HMGB1), caspase3 as well as SHP2:phospho-SHP2, extracellular-regulated kinase (Erk1/2): phospho-Erk1/2, and signal transducer and activator of transcription 3 (STAT3):phospho-STAT3 protein in kidney tissues were detected by Western blotting. The levels of creatinine (Cre) and blood urea nitrogen (BUN) in serum were measured according to the manufacturer's instructions. Blood inflammatory cytokine/chemokine levels were detected by ELISA. RESULTS: We found that indices of kidney injury, including levels of BUN, Cre and NGAL as well as histopathologic changes, were significantly increased after Hem/CLP in comparison with that in the S/S group. Furthermore, Hem/CLP resulted in elevated serum levels of inflammatory cytokines/chemokines, and induced increased levels of HMGB1, SHP2:phospho-SHP2, Erk1/2:phospho-Erk1/2, and STAT3:phospho-STAT3 protein expression in the kidney. Treatment with PHPS1 markedly attenuated these Hem/CLP-induced changes. CONCLUSIONS: In conclusion, our data indicate that SHP2 inhibition attenuates AKI induced by our double-hit/sequential insult model of Hem/CLP and that this protective action may be attributable to its ability to mitigate activation of the Erk1/2 and STAT3 signaling pathway. We believe this is a potentially important finding with clinical implications warranting further investigation.

Effect of Dexmedetomidine on duration of mechanical ventilation in septic patients: a systematic review and meta-analysis.

BACKGROUND: Because of its analgesic and light sedative properties, the highly selective alpha-2 adrenergic receptor agonist dexmedetomidine (DEX) has been suggested for the treatment of septic patients, but its effect on the duration of mechanical ventilation remains unclear. The present study was conducted to review the extant literature in DEX and determine its influence on ventilation time in adult septic patients. METHODS: Databases of PubMed, Cochrane, and EMBASE were applied till 20th January 2019 without language restriction. The searching strategy as following: sepsis OR septic AND mechanical ventilation AND dexmedetomidine. Two authors screened titles, abstracts, and even articles to meet the including criterion independently. In addition, references of related articles or reviews were also referred. Data was recorded in a table and analyzed using the software of Review Manager 5.0. RESULTS: Four studies with a total of 349 patients were included. Three trials with 267 patients revealed the effect of DEX on duration of mechanical ventilation, two trials with 264 patients on ventilator-free days and four trials with 334 patients on 28-day mortality. The analyzed results indicated that DEX was not associated with significantly different durations of mechanical ventilation (MD 0.65, 95% CI, - 0.13 to 1.42, P = 0.10). However, there were significant differences in ventilator-free days (MD 3.57, 95% CI, 0.26 to 6.89, P = 0.03) and 28-day mortality (RR 0.61, 95% CI, 0.49 to 0.94, P = 0.02) in the septic patients. CONCLUSION: Administration of DEX for sedation in septic patients was not associated with the duration of mechanical ventilation, but it increased the ventilator-free days and reduced 28-day mortality.

Salidroside rescued mice from experimental sepsis through anti-inflammatory and anti-apoptosis effects.

BACKGROUND: Salidroside (SDS) is the main effective component of Rhodiola rosea L with a variety of pharmacologic properties. The objective of this study was to investigate the efficacy of SDS in the treatment of experimental sepsis in mice and explore the possible underlying action mechanisms. METHODS: Sepsis was induced in C57BL/6 male mice via cecal ligation and puncture (CLP). The animals were divided into three groups as follows: sham, CLP, and CLP plus SDS. SDS (50 mg/kg) was injected intraperitoneally 1 h after operation. Postoperative survival of the mice, bacterial clearance in blood and peritoneal lavage fluid, cytokine secretion in blood, and histology of lung were evaluated. In addition, apoptosis of immune cells in the spleen and thymus were examined, respectively. RESULTS: SDS administration prolonged the survival of the septic mice, inhibited the proinflammatory responses, and enhanced bacterial clearance. It also alleviated the pathologic changes in the lung and inhibited the apoptosis of immune cells in the spleen and thymus after CLP challenge. CONCLUSIONS: SDS exerts a protective effect in CLP-induced sepsis by attenuating the proinflammatory responses, enhancing bacterial clearance, and preserving adaptive immunity. SDS may be a promising therapeutic strategy for the treatment of sepsis.

Ginsenoside Rg1 protects mouse liver against ischemia-reperfusion injury through anti-inflammatory and anti-apoptosis properties.

BACKGROUND: Ginsenoside Rg1, the major effective component of ginseng, possesses a variety of pharmacologic activities. The objective of this study was to investigate the effects of Rg1 on liver ischemia-reperfusion (IR) injury and explore its potential mechanisms. MATERIALS AND METHODS: Liver warm IR injury was achieved by occluding the portal vein and hepatic artery for 1 h followed by 6-h reperfusion. Eighteen mice were equally randomized into three groups: sham group, IR group, and IR plus Rg1 group (n = 6 mice per group). Mice received an intravenous dose of 20 mg/kg Rg1 or an equivalent volume of saline before ischemic insult. Liver samples and serum were collected for analyses. Serum aminotransferase, histopathology, and apoptosis were determined. Cytokines were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The phosphorylation of nuclear factor kappa B (NF-κB) p65 was assessed by Western blotting. In addition, the effect of Rg1 in a simulated IR model in vitro was also investigated. Rg1 (100 ug/mL and 500 ug/mL) was administered 1 h before hypoxia insult, and then apoptosis was measured after 12-h reperfusion. RESULTS: Liver IR injury led to a dramatic increase in aminopherase activity, apoptosis and necrosis of hepatocytes, and production of proinflammatory cytokines. Pretreatment with Rg1 protected mice from IR-induced liver injury. Treatment with a high-dose Rg1 (500 ug/mL) significantly suppressed apoptosis compared with a lower dose or control (both P < 0.001). Phosphorylation of NF-κB p65 was increased significantly in IR group, and administration with Rg1 suppressed the level of phosphorylation. CONCLUSIONS: Pretreatment of mice with Rg1 reduced hepatocellular apoptosis and inhibited inflammatory response, which was in part through the NF-κB signaling pathway. Rg1 may provide a novel therapeutic strategy for the treatment of IR-induced liver injury.

Salidroside attenuates concanavalin A-induced hepatitis via modulating cytokines secretion and lymphocyte migration in mice.

Salidroside, isolated from the medicinal plant Rhodiola, was reported to serve as an "adaptogen." This study was designed to explore the protective effect of salidroside on concanavalin A- (Con A-) induced hepatitis in mice and investigate potential mechanisms. C57BL/6 mice were randomly divided into control group, Con A group, and salidroside group. Salidroside (50 mg/kg) was injected intravenously followed by Con A administration. The levels of ALT, AST, inflammatory cytokines and CXCL-10 were examined. The pathological damage of livers was assessed, the amounts of phosphorylated IκBα and p65 were measured, and the numbers of CD4(+) and CD8(+) T lymphocytes in the blood, spleen and infiltrated in the liver were calculated. Our results showed that salidroside pretreatment reduced the levels of ALT, AST dramatically and suppressed the secretion of proinflammatory cytokines through downregulating the activity of NF-κB partly. Salidroside altered the distribution of CD4(+) and CD8(+) T lymphocyte in the liver and spleen through regulating CXCL-10 and decreased the severity of liver injuries. In conclusion, these results confirm the efficacy of salidroside in the prevention of immune mediated hepatitis in mice.

The role of TIM-3 in sepsis: a promising target for immunotherapy?

Sepsis remains a significant cause of mortality and morbidity worldwide, with limited effective treatment options. The T-cell immunoglobulin and mucin domain-containing molecule 3 (TIM-3) has emerged as a potential therapeutic target in various immune-related disorders. This narrative review aims to explore the role of TIM-3 in sepsis and evaluate its potential as a promising target for immunotherapy. We discuss the dynamic expression patterns of TIM-3 during sepsis and its involvement in regulating immune responses. Furthermore, we examine the preclinical studies investigating the regulation of TIM-3 signaling pathways in septic models, highlighting the potential therapeutic benefits and challenges associated with targeting TIM-3. Overall, this review emphasizes the importance of TIM-3 in sepsis pathogenesis and underscores the promising prospects of TIM-3-based immunotherapy as a potential strategy to combat this life-threatening condition.

Exploring the gut microbiome-Postoperative Cognitive Dysfunction connection: Mechanisms, clinical implications, and future directions.

Postoperative Cognitive Dysfunction (POCD) is a common yet poorly understood complication of surgery that can lead to long-term cognitive decline. The gut-brain axis, a bidirectional communication system between the central nervous system and the gut microbiota, plays a significant role in maintaining cognitive health. The potential for anesthetic agents and perioperative medications to modulate the gut microbiota and influence the trajectory of POCD suggests the need for a more integrated approach in perioperative care. Perioperative medications, including opioids and antibiotics, further compound these disruptions, leading to dysbiosis and consequent systemic and neuroinflammation implicated in cognitive impairment. Understanding how surgical interventions and associated treatments affect this relationship is crucial for developing strategies to reduce the incidence of POCD. Strategies to preserve and promote a healthy gut microbiome may mitigate the risk and severity of POCD. Future research should aim to clarify the mechanisms linking gut flora alterations to cognitive outcomes and explore targeted interventions, such as probiotic supplementation and microbiota-friendly prescription practices, to safeguard cognitive function postoperatively.

Methane-rich saline protects against sepsis-associated cognitive deficits in mice.

Sepsis is associated with multiple organ dysfunction, and the brain is particularly vulnerable. Sepsis-associated encephalopathy (SAE) increases the mortality of patients with sepsis; however, the pathogenesis of SAE remains unclear. Methane, the simplest aliphatic hydrocarbon, has been reported to have anti-inflammatory and organ-protective effects. This study aimed to investigate the effects of methane on the cognitive deficits in mice with experimental sepsis. We randomly divided C57BL/6 male mice into sham, cecal ligation and puncture (CLP), and CLP + methane-rich saline (MS) groups. Twenty-four hours after surgery, behavioral tests were conducted on surviving mice and the hippocampus were collected for biochemical analysis. We found that CLP resulted in cognitive deficits in septic mice. A physiological mechanistic investigation revealed that microglia in the hippocampus are largely activated, coupled with the production of inflammatory cytokines and reactive oxygen species (ROS). Notably, methane inhibited the activation of microglia in the hippocampus, reduced the severity of inflammation, diminished the generation of ROS, and ultimately alleviated behavioral impairment in septic mice. Together, these show that treatment with methane ameliorated cognitive deficits in septic mice, which is partly related to the anti-inflammatory and antioxidative effects in the hippocampus.

Butorphanol alleviates lipopolysaccharide-induced inflammation and apoptosis of cardiomyocytes via activation of the κ-opioid receptor.

Sepsis-induced myocardial dysfunction is a leading cause of the high mortality rates associated with sepsis. The aim of the present study was to investigate the effect of butorphanol on sepsis-induced cardiomyocyte dysfunction. Lipopolysaccharide (LPS) was used to induce H9C2 cardiomyocytes to establish an in vitro sepsis model. The effect of butorphanol on the viability of LPS-induced H9C2 cells was analyzed using a Cell Counting Kit-8 assay. The levels of tumor necrosis factor-α, interleukin (IL)-1ß and IL-6 were detected using ELISA. Western blotting was used to analyze the expression levels of inflammation-and apoptosis-related proteins. Cell apoptosis was measured using a TUNEL assay. The expression levels of κ-opioid receptor (KOR) were analyzed using reverse transcription-quantitative PCR analysis and western blotting. Following LPS induction, the levels of inflammatory cytokines and proapoptotic proteins were found to be upregulated in H9C2 cells, while butorphanol treatment downregulated these levels. The expression levels of KOR were also upregulated following butorphanol treatment in LPS-induced H9C2 cells. Addition of the KOR inhibitor, nor-binaltorphimine, alleviated the inhibitory effects of butorphanol on inflammation and apoptosis in LPS-induced H9C2 cells. In conclusion, the findings of the present study provided evidence indicating that butorphanol may alleviate LPS-induced inflammation and apoptosis in cardiomyocytes by upregulating KOR expression, which may provide a novel insight into the potential therapeutic effects of butorphanol and its underlying mechanism of action.

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway.

BACKGROUND: To investigate the neuroprotective effect of edaravone on excessive-dose propofol-induced neurotoxicity in the hippocampus of newborn rats and HT22 cells. METHODS: Cell proliferation was investigated by assessing ki67 expression in the neural stem of the hippocampus of newborn rats and by cell counting kit-8 (CCK8) assay in HT22 cells. Cell apoptosis was assessed in vivo by caspase 3 detection in Western blots and measurement of apoptosis in neurons and glial cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Apoptosis was analyzed by flow cytometry in HT22 cells. The Morris water maze was used to evaluate the long-term learning and memory ability of rats. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). The expression of mBDNF/TrkB/PI3K pathway-related proteins was detected by Western blot and quantitative reverse transcription-polymerase chain reaction (q-RT PCR). RESULTS: In neonatal rat hippocampus and HT22 cells, edaravone increased cell proliferation and decreased cell apoptosis after excessive propofol-induced neurotoxicity. In addition, the levels of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α were reduced by edaravone pretreatment. The use of the tropomyosin receptor kinase B (TrkB) antagonist ANA-12 and TrkB agonist 7,8DHF with propofol groups showed that edaravone mitigated excessive propofol-induced neurotoxicity through the mature brain-derived neurotrophic factor (mBDNF)/TrkB/phosphoinositide 3-kinase (PI3K) pathway. However, the current dose of propofol did not significantly affect long-term learning and memory in rats. CONCLUSION: Edaravone pretreatment ameliorated propofol-induced proliferation inhibition, neuroapoptosis, and neural inflammation by activating the mBDNF/TrkB/PI3K pathway.

Shape and size controlled synthesis of anatase nanocrystals with the assistance of ionic liquid.

We report an ionic liquid (IL) assisted hydrothermal method to synthesize anatase TiO(2) nanocrystals (NCs), in which TiCl(4) was used as precursor, 1-butyl-3-methylimidazolium chloride (bmim(+)Cl(-)) as IL, and F(-) or SO(4)(2-) ions as phase transformation inhibitor. The surfactant-like nature of IL was found to play a key role in controlling the crystallization process via controlling the aggregation manner of the NCs. The fine-tuning abilities of the operating parameters of the bmim(+)Cl(-)/TiCl(4)/H(2)O system facilitated the controlling over the shape and size of TiO(2) NCs. Phase-pure anatase monodisperse NCs with various shape and size were controllably obtained. Moreover, the aggregation manners of anatase NCs were also studied, and it was demonstrated that the high concentration of HF or H(2)SO(4) could result in aggregation of anatase NCs to form pseudo single crystals.

Study on the anatase to rutile phase transformation and controlled synthesis of rutile nanocrystals with the assistance of ionic liquid.

We developed a route to synthesize rutile TiO(2) nanocrystals (NCs) with the assistance of 1-butyl-3-methylimidazolium chloride (bmim(+)Cl(-)). The phase transformation from anatase to rutile phase was investigated, and a simple model to describe the phase transformation process was proposed considering that the nucleation and growth of rutile phase were determined by the aggregation manner of anatase NCs and Ostwald ripening process, respectively. It was demonstrated that the surfactant-like nature of the IL used was crucial for controlling the crystallization process via controlling the aggregation manner of the NCs. The phase, shape, and size of TiO(2) NCs could be tuned by the controlling the operating conditions, such as temperature, solution acidity, and reactant concentration of the bmim(+)Cl(-)/TiCl(4)/H(2)O reaction system. Phase-pure rutile multipods and 1D nanorods with different sizes were controllably obtained.

The dispersion of carbon nanotubes in water with the aid of very small amounts of ionic liquid.

Multiwalled carbon nanotubes can be dispersed stably in water with the aid of a very small amount of 1-aminoethyl-3-methylimidazolium bromide ([C(2)NH(2)mim][Br]) or 1-(2-aminoethyl) pyridinium bromide ([C(2)NH(2)py][Br]).

Preparation of a polyurethane electret nanofiber membrane and its air-filtration performance.

Pollution by atmospheric particulate matter (PM) is a serious threat to human health, and traditional window screens are unable to intercept fine particles. Therefore, it is urgent to develop anti-haze window screens to effectively protect the public. We prepared a polyurethane/silicon nitride (PU/Si3N4) electret nanofiber membrane with a minimum diameter (350 nm) and narrower diameter distribution than those of PU-Boehmite, PU-SiO2, and PU-TiO2 membranes by electrospinning. The PU-Si3N4 fiber membrane has good mechanical properties with stress of 18.05 MPa and strain of 170%. Moreover, PU/Si3N4 exhibits a maximum current peak (2.63 pA) at 90 °C. Importantly, PU/Si3N4 membranes applied to window screens still maintain high filtration efficiency (79.36%) and low resistance (25 Pa) to air flow at a low areal density of 1.22 g/m2. Furthermore, they show good light transmittance (40%) and air permeability (46.42 mm s-1). Therefore, PU/Si3N4 electret nanofiber window screens have broad application prospects.

Anti-CD200 attenuates concanavalin A induced hepatitis via modulating the imbalance of CD4+ T lymphocyte differentiation in mice.

Hepatitis occurs in critical ill patients with bad morbidity and mortality. It is known that imbalance of Th1 and Th2 lymphocytes differentiations plays a key role in its mechanisms. Recent studies indicated that type 1 membrane glycoprotein CD200 serves as co-inhibitory molecule, negatively regulating the immune response. In regard of this, we used Concanavalin A (Con A) induced liver injury model to research the effect of CD200 on the differentiation of CD4+ T lymphocyte and found that the expression of CD200 on CD4+ T was significantly higher in hepatitis mouse. The apoptosis of CD4+ T cell in Con A induced liver injury was significantly attenuated by anti-CD200. The concentration of solube IL-2 and IFN-γ was reduced by anti-CD200, in addition, the expression of T-bet, GATA3 and FoxP3 mRNA were all attenuated by anti-CD200. The phosphorylation of SH-2 containing inositol 5' polyphosphatase 1 (SHIP1) was significantly increased in Con A induced liver injury and reduced by anti-CD200. We hypothesized that, anti-CD200 inhibited the phosphorylation of SHIP1, the expression of T-bet, GATA3 and FoxP3 mRNA and CD4+ T differentiation to protect the liver from autoimmune hepatitis.

Lugrandoside attenuates LPS-induced acute respiratory distress syndrome by anti-inflammation and anti-apoptosis in mice.

This study aimed to investigate the protective effects and specific mechanisms of lugrandoside (LG) on lipopolysaccharides (LPS)-induced acute respiratory distress syndrome (ARDS). LG is a novel phenylpropanoid glycoside with many biological properties, isolated from the culinary leaves of Digitalis lutea L. and Digitalis grandiflora Miller. The primary indicators to assess the lung injury were infiltration of inflammatory cells; pulmonary edema; expression of proinflammatory cytokines, cyclo-oxygenase 2, and intracellular adhesion molecule 1; activation of nuclear factor-κB pathways; and cellular apoptosis. The results showed that LG evidently alleviated the inflammatory response, decreased the apoptosis of alveolar macrophages, and improved the lung injury in mice with LPS-induced ARDS. In conclusion, LG improved LPS-induced ARDS by anti-inflammation and anti-apoptosis and might be a promising pharmacological therapy for ARDS.