Porous Zinc Oxide and Plant Polyphenols as a Replacement for High-Dose Zinc Oxide on Growth Performance, Diarrhea Incidence, Intestinal Morphology and Microbial Diversity of Weaned Piglets.

The aim of this experiment is to evaluate the effects of adding porous zinc oxide, plant polyphenols, and their combination to diets without antibiotics and high-dose zinc oxide on the growth performance, diarrhea incidence, intestinal morphology, and microbial diversity of weaned piglets. A total of 150 Duroc × Landrace × Large White weaned piglets were allocated to one of five diets in a randomized complete block design with six replicates and five piglets per replicate. The experimental period was 42 d, divided into two feeding stages: pre-starter (0-14 d) and starter (14-42 d). In the pre-starter stage, the negative control group (NC) was fed a basal diet, the positive control group (PC) was fed a basal diet with 2000 mg/kg of zinc oxide, the porous zinc oxide group (PZ) was fed a basal diet with 500 mg/kg of porous zinc oxide, the plant polyphenol group (PP) was fed a basal diet with 1500 mg/kg of plant polyphenols, and the combination group (PZ + PP) was fed a basal diet with 500 mg/kg of porous zinc oxide and 1500 mg/kg of plant polyphenols. In the starter stage, the NC, PC, and PZ groups were fed a basal diet, while the PP and PZ + PP groups were fed a basal diet with 1000 mg/kg of plant polyphenols. The results showed that, (1) compared with the PZ group, adding plant polyphenols to the diet showed a trend of increasing the ADFI of weaned piglets from 14 to 28 d (p = 0.099). From days 28 to 42 and days 0 to 42, porous zinc oxide and the combination of porous zinc oxide and plant polyphenols added to the control diet improved the FCR to the level observed in pigs fed the PC diet. (2) Dietary PZ + PP tended to increase the jejunal villus height (VH) of weaned piglets (p = 0.055), and significantly increased the villus-height-to-crypt-depth ratio compared to the NC group (p < 0.05). (3) Compared with the NC group, PZ supplementation decreased the relative abundance of Firmicutes and increased the relative abundance of Bacteroidetes, and the relative abundance of Lactobacillus in the PZ and PZ + PP groups were both increased. In conclusion, porous zinc oxide and plant polyphenols may have synergistic effects in modulating intestinal health in weaned piglets and be a potential alternative to high-dose zinc oxide.

Evaluation of Available Energy and Standardized Ileal Digestibility of Amino Acids in Fermented Flaxseed Meal for Growing Pigs.

Flaxseed meal (FSM) is a byproduct of flaxseed oil extraction which has rich nutritional value and can be used as a high-quality new protein ingredient. However, the anti-nutrient factor (ANF) in FSM restricts its potential application in feed. The strategy of microbial fermentation is a highly effective approach to reducing ANF in FSM and enhancing its feeding value. However, evaluation of the nutritional value of fermented flaxseed meal (FFSM) in growing pigs has not yet been conducted. Thus, the purpose of this study was to investigate the nutritional value of FFSM in growing pigs and comparison of the effect of fermentation treatment on improving the nutritional value of FSM. Two experiments were conducted to determine the available energy value, apparent digestibility of nutrients, and standard ileal digestibility of amino acids of FSM and FFSM in growing pigs. The results showed as follows: (1) Fermentation treatment increased the levels of crude protein (CP), Ca and P in FSM by 2.86%, 9.54% and 4.56%, while decreasing the concentration of neutral detergent fiber (NDF) and acid detergent fiber (ADF) by 34.09% and 12.71%, respectively (p < 0.05); The degradation rate of CGs in FSM was 54.09% (p < 0.05); (2) The digestible energy (DE) and metabolic energy (ME) of FSM and FFSM were 14.54 MJ/kg, 16.68 MJ/kg and 12.85 MJ/kg, 15.24 MJ/kg, respectively; (3) Compared with FSM, dietary FFSM supplementation significantly increased the apparent digestibility of CP, NDF, ADF, Ca, and P of growing pigs (p < 0.05) and significantly increased the standard ileal digestibility of methionine (p < 0.05). These results indicate that fermentation treatment could effectively enhance the nutritional value of FSM and provide basic theoretical data for the application of FFSM in pig production.

Rosa laevigata Michx. Polysaccharide Ameliorates Diabetic Nephropathy in Mice through Inhibiting Ferroptosis and PI3K/AKT Pathway-Mediated Apoptosis and Modulating Tryptophan Metabolism.

Diabetic nephropathy (DN) is a metabolic disease wherein chronic hyperglycemia triggers various renal cell dysfunctions, eventually leading to progressive kidney failure. Rosa laevigata Michx. is a traditional Chinese herbal medicine. Many studies have confirmed its antioxidative, anti-inflammatory, and renoprotective effects. However, the effects and mechanisms of Rosa laevigata Michx. polysaccharide (RLP) in DN remain unclear. In this study, a DN mouse model was established to investigate the therapeutic effect of RLP on DN mice. Then, nontargeted metabolomics was used to analyze the potential mechanism of RLP in the treatment of DN. Finally, the effects of RLP on ferroptosis and the PI3K/AKT pathway were investigated. The results demonstrated that RLP effectively alleviated renal injury and reduced inflammation and oxidative stress in the kidney. In addition, nontargeted metabolomic analysis indicated that RLP could modulate riboflavin metabolism and tryptophan metabolism in DN mice. Notably, ferroptosis and PI3K/AKT pathway-mediated apoptosis in the kidney were also ameliorated following RLP treatment. In conclusion, this study confirmed that RLP had a significant therapeutic effect on DN mice. Furthermore, RLP treatment modulated tryptophan metabolism and inhibited ferroptosis and PI3K/AKT pathway-mediated apoptosis in the kidney.

Dietary Supplementation with Different Types of Potassium and Magnesium during Late Gestation and Lactation Modulates the Reproductive Performance, Antioxidant Capacity, and Immune Function of Sows.

The objective of this study was to investigate the effects of dietary supplementation with different types of potassium and magnesium on the reproductive performance, antioxidant capacity, and immunity of sows. Forty-five Landrace × Yorkshire sows at the late gestation stage (85 d) were randomly assigned to three groups (n = 15). Sows in the control group (CON), potassium chloride and magnesium sulfate group (PM), and potassium-magnesium sulfate group (PMS) were fed with a basal diet, a basal diet supplemented with magnesium sulfate (0.20%) and potassium chloride (0.15%), or a basal diet supplemented with potassium-magnesium sulfate (0.45%), respectively. The results showed that dietary supplementation with PMS did not yield significant effects on the reproductive performance compared with the CON group (p > 0.05). However, it significantly elevated the level of insulin-like growth factor 1 (IGF-1) in plasma and immunoglobulin A (IgA) in colostrum (p < 0.05). Furthermore, PMS significantly augmented the activities of catalase (CAT) and superoxide dismutase (SOD) while reducing the levels of malondialdehyde (MDA) in comparison to the CON group (p < 0.05). Compared with the PM group, the PMS group significantly reduced the incidence rate of intrauterine growth restriction (IUGR) (p < 0.05) and significantly decreased the concentration of the proinflammatory cytokine (TNF-α) level in plasma (p < 0.05). These results indicated that dietary supplementation with PMS during late gestation could enhance sows' antioxidant capacity and the IgA level in colostrum. These findings will provide a theoretical reference for the use of magnesium and potassium in sow production to improve sows' health.

Low-temperature plasma modification, structural characterization and anti-diabetic activity of an apricot pectic polysaccharide.

To fully research the anti-diabetic activity of apricot polysaccharide, low temperature plasma (LTP) was used to modify apricot polysaccharide. The modified polysaccharide was isolated and purified using column chromatography. It was found that LTP modification can significantly improve the α-glucosidase glucosidase inhibition rate of apricot polysaccharides. The isolated fraction FAPP-2D with HG domain showed excellent anti-diabetic activity in insulin resistance model in L6 cell. We found that FAPP-2D increased the ADP/ATP ratio and inhibited PKA phosphorylation, activating the LKB1-AMPK pathway. Moreover, FAPP-2D activated AMPK-PGC1α pathway, which could stimulated mitochondrial production and regulate energy metabolism, promoting GLUT4 protein transport to achieve an anti-diabetic effect. The Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy data showed that the LTP modification could increase the CH bond content while decreasing the C-O-C/C-O bond content, indicating that LTP destroyed the C-O-C/C-O bond, which enhanced the anti-diabetes activity of the modified apricot pectin polysaccharide. Our findings could pave the way for the molecular exploitation of apricot polysaccharides and the application of low-temperature plasma.

Multi-component immune knockout: A strategy for studying the effective components of traditional Chinese medicine.

Periploca forrestii Schltr., a traditional Chinese medicine (TCM), is commonly used to treat autoimmune diseases such as rheumatoid arthritis (RA). However, its mechanism, involving a variety of cardiac glycosides, remains largely unknown. The immune knockout strategy can highly selectively deplete target components by immunoaffinity chromatography (IAC). We aimed to identify the common structural features of cardiac glycosides in P. forrestii and design IAC to specifically recognize these features to achieve the multi-component knockout of potential active substances from the extracts of P. forrestii. A content detection experiment confirmed that the content of a compound with periplogenin structure (CPS) in the extract of P. forrestii was reduced by 45% by IAC of periplogenin. The immunosuppressive ability of the extract on H9 human T lymphocytic cells was weakened after CPS knockout from P. forrestii extract. Molecular biology experiments showed that mRNA expression of interferon-γ (IFN-γ), interleukin-2 (IL-2), and interleukin-6 (IL-6) in H9 cells was up-regulated after CPS knockout, while no significant changes in the expression of interleukin-4 (IL-4) were found. CPS knockout from P. forrestii extract did not cause significant changes in the proliferation of lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells incubated with this extract. These results indicate that CPS exhibited immunosuppressive effects via inhibiting the T helper 1 (Th1) cell immune response and not via the anti-inflammatory components in P. forrestii. This is the first use of IAC to achieve multi-component knockout in TCM extracts for identifying effective compounds. This method is effective and reliable and warrants further exploration.

Tetrandrine inhibits proliferation of colon cancer cells by BMP9/ PTEN/ PI3K/AKT signaling.

Despite advances in screening and treatment, colon cancer remains one of the leading causes of cancer-related death. Finding novel and useful drug treatment targets is also an urgent need for clinical applications. Tetrandrine (Tet) is extracted from the Chinese medicinal herbal medicine, which is a well-known calcium blocker with a variety of pharmacological activities, including anti-cancer. In this study, we recruited cell viability assay, flow cytometry analysis, cloning formation to confirm that Tet can inhibit the proliferation of SW620 cells, and induce apoptosis. Mechanically, we confirmed that Tet up-regulates the mRNA and protein level of BMP9 in SW620 cells. Over-expression BMP9 enhances the anti-cancer effects of Tet in SW620 cells, but these effects can be partly reversed by silencing BMP9. Also, Tet reduces phosphorylation of Aktl/2/3 in SW620 cells, which could be elevated by overexpressed BMP9 and impaired by silencing BMP9. Furthermore, we demonstrated that Tet reduces phosphorylated PTEN, which can be promoted by overexpressed BMP9, analogously also be attenuated through silencing BMP9. Finally, we introduced a xenograft tumor model to investigate the anti-proliferative effect of Tet, further to explore the effects of BMP9 and PTEN in SW620 cells. Our findings suggested that the anti-cancer activity of Tet in SW620 cells may be mediated partly by up-regulating BMP9, followed by inactivation PI3K/Akt through up-regulating PTEN at least.

Selenium Deficiency-Induced Pancreatic Pathology Is Associated with Oxidative Stress and Energy Metabolism Disequilibrium.

Selenium (Se) is an essential micronutrient that plays a crucial role in development and physiological processes. The present study aimed to investigate the effects of Se deficiency on pancreatic pathology and the potential mechanism in pigs. Twenty-four castrated male Yorkshire pigs were divided into two groups and fed a Se-deficient diet (0.007 mg Se/kg) or a Se-adequate diet (0.3 mg Se/kg) for 16 weeks. The serum concentrations of insulin and glucagon, Se concentration, histologic characteristics, apoptotic status, antioxidant activity, free radical content, and major metabolite concentrations were analyzed. The results showed that Se deficiency reduced the concentrations of insulin and glucagon in the serum and of Se in pancreas, decreased the number of islets and cells in the local islets, and induced pancreatic apoptosis. Se deficiency caused a redox imbalance, which led to an increase in the content of free radicals and decreased the activity of antioxidant enzymes. Of 147 targeted metabolites judged to be present in pancreas, only hypotaurine and D-glucuronic acid had differential concentrations with the false discovery rate < 0.05. Pathway analysis using metabolites with differential expression (unadjusted P < 0.05, fold change > 1.4 or < 0.67) found that 8 glycolytic metabolites were significantly increased by Se-deficient, whereas most of the tricarboxylic acid cycle and pentose phosphate pathway metabolites were not significantly changed. Our studies indicated that Se deficiency-induced pancreatic pathology was associated with oxidative stress and enhanced activity of glycolysis, which may provide gaining insight into the actions of Se as a diabetogenic factor.

Selenium supplementation protects against oxidative stress-induced cardiomyocyte cell cycle arrest through activation of PI3K/AKT.

Oxidative stress significantly contributes to heart disease, and thus might be a promising target for ameliorating heart failure. Mounting evidence suggests that selenium has chemotherapeutic potential for treating heart disease due to its regulation of selenoproteins, which play antioxidant regulatory roles. Oxidative stress-induced cardiomyocyte cell cycle arrest contributes to the loss of cardiomyocytes during heart failure. The protective effects and mechanism of selenium against oxidative stress-induced cell cycle arrest in cardiomyocytes warrant further study. H9c2 rat cardiomyoblast cells were treated with hydrogen peroxide in the presence or absence of selenium supplementation. Na2SeO3 pretreatment alleviated H2O2-induced oxidative stress, increased thioredoxin reductase (TXNRD) activity and glutathione peroxidase (GPx) activity and counteracted the H2O2-induced cell cycle arrest at the S phase. These effects were accompanied by attenuation of the H2O2-induced strengthening of the G2/M-phase inhibitory system, including increased mRNA and protein levels of cyclin-dependent kinase 1 (CDK1) and decreased p21 mRNA levels. Notably, Na2SeO3 pretreatment activated the PI3K/AKT signaling pathway, and inhibition of PI3K counteracted the protective effects of selenium on H2O2-induced cell cycle arrest. We corroborated our findings in vivo by inducing oxidative stress in pig heart by feeding a selenium deficient diet, which decreased the TXNRD activity, inactivated PI3K/AKT signaling and strengthened the G2/M-phase inhibitory system. We concluded that the cardioprotective effects of selenium supplementation against oxidative stress-induced cell cycle arrest in cardiomyocytes might be mediated by the selenoprotein-associated (GPx and TXNRD) antioxidant capacity, thereby activating redox status-associated PI3K/AKT pathways, which promote cell cycle progression by targeting the G2/M phase inhibitory system. This study provides new insight into the underlying mechanisms of cardioprotection effects of selenium at the cellular level.

Se deficiency induces renal pathological changes by regulating selenoprotein expression, disrupting redox balance, and activating inflammation.

Selenium (Se) is closely associated with kidney disease, and renal injury often occurs together with hyposelenemia. This study was designed to reveal the mechanism underlying renal injury induced by Se deficiency in pigs. Twenty-four castrated male Yorkshire pigs were divided into two groups fed either a Se-deficient diet (0.007 mg Se per kg) or a Se-adequate diet (0.3 mg Se per kg). Serum and kidney samples were collected at the 16th week of the trial, processed, and analyzed for serum biochemistry, Se concentration, kidney index markers, histology, selenoprotein mRNA expression, redox status, and inflammatory cytokines. Dietary Se deficiency induced kidney injury, decreased (P < 0.05) Se concentrations, and increased (P < 0.05) kidney index and serum blood urea nitrogen, creatinine, and carbon dioxide values. Histological analysis indicated that Se deficiency induced inflammatory lesions and renal tubular atrophy in the renal medulla. Se deficiency downregulated (P < 0.05) nine selenoprotein genes (GPX1, SELENOW, SELENOH, SELENOP, GPX3, TXNRD2, SELENOI, SELENON, and SELENOM) and upregulated (P < 0.05) SEPHS2 in the kidneys. Se deficiency decreased (P < 0.05) the activity of glutathione peroxidase, thioredoxin reductase, and catalase, as well as the hydroxyl radical inhibition capacity, and increased (P < 0.05) the content of malondialdehyde and nitric oxide. Se deficiency increased (P < 0.05) the expression of the transcription factors NF-κB and HIF-1α, and regulated inflammatory cytokines. Se deficiency increased (P < 0.05) the expression of IL-6, IL-8, IL-12, IL-17, and cyclooxygenase-2, and decreased (P < 0.05) the expression of IL-10, IL-13, and TGF-ß. These results indicated that Se deficiency induces kidney injury through the regulation of selenoproteins, oxidative stress, and inflammation.

Targeted Metabolomics Analysis Reveals that Dietary Supranutritional Selenium Regulates Sugar and Acylcarnitine Metabolism Homeostasis in Pig Liver.

BACKGROUND: The association between high selenium (Se) intake and metabolic disorders such as type 2 diabetes has raised great concern, but the underlying mechanism remains unclear. OBJECTIVE: Through targeted metabolomics analysis, we examined the liver sugar and acylcarnitine metabolism responses to supranutritional selenomethionine (SeMet) supplementation in pigs. METHODS: Thirty-six castrated male pigs (Duroc-Landrace-Yorkshire, 62.0 ± 3.3 kg) were fed SeMet adequate (Se-A, 0.25 mg Se/kg) or SeMet supranutritional (Se-S, 2.5 mg Se/kg) diets for 60 d. The Se concentration, biochemical, gene expression, enzyme activity, and energy-targeted metabolite profiles were analyzed. RESULTS: The Se-S group had greater fasting serum concentrations of glucose (1.9-fold), insulin (1.4-fold), and free fatty acids (FFAs,1.3-fold) relative to the Se-A group (P < 0.05). The liver total Se concentration was 4.2-fold that of the Se-A group in the Se-S group (P < 0.05), but expression of most selenoprotein genes and selenoenzyme activity did not differ between the 2 groups. Seven of 27 targeted sugar metabolites and 4 of 21 acylcarnitine metabolites significantly changed in response to high SeMet (P < 0.05). High SeMet supplementation significantly upregulated phosphoenolpyruvate carboxy kinase (PEPCK) activity by 64.4% and decreased hexokinase and succinate dehydrogenase (SDH) activity by 46.5-56.7% (P < 0.05). The relative contents of glucose, dihydroxyacetone phosphate, α-ketoglutarate, fumarate, malate, erythrose-4-phosphate, and sedoheptulose-7-phosphate in the Se-S group were 21.1-360% greater than those in the Se-A group (P < 0.05). The expression of fatty acid synthase (FASN) and the relative contents of carnitine, hexanoyl-carnitine, decanoyl-carnitine, and tetradecanoyl-carnitine in the Se-S group were 35-97% higher than those in the Se-A group (P < 0.05). CONCLUSIONS: Dietary high SeMet-induced hyperglycemia and hyperinsulinemia were associated with suppression of sugar metabolism and elevation of lipid synthesis in pig livers. Our research provides novel insights into high SeMet intake-induced type 2 diabetes.

Plasma nesfatin-1 level in obese patients after acupuncture: a randomised controlled trial.

BACKGROUND: Nesfatin-1 is an anorexigenic hormone suggested to regulate obesity. OBJECTIVE: To investigate the relationship between nesfatin-1 level and anthropometric and metabolic parameters in obese patients, and examine the change in plasma nesfatin-1 level after acupuncture treatment. METHODS: 64 obese adult patients without diabetes and 58 normal weight control subjects were enrolled in this study. The obese patients were randomly divided into an acupuncture plus diet group (n=32) and a diet only group (n=32). Measurements were repeated after 45 days. RESULTS: Body mass index (BMI), waist and hip circumferences, serum insulin, lipoprotein and insulin resistance measures were significantly higher, and plasma nesfatin-1 level was significantly lower, in obese patients than in normal weight controls. In addition, negative correlations were found between plasma nesfatin-1 level and BMI, waist and hip circumferences. Weight reduction in participants after acupuncture and diet restriction was 7.0% and 4.3%, respectively. Plasma nesfatin-1 level increased from 2.75±1.16 to 3.44±1.28 ng/mL and from 2.86±1.07 to 3.23±1.06 ng/mL in acupuncture and diet groups, respectively; the difference was significant, p<0.05. CONCLUSIONS: Plasma nesfatin-1 level is reduced in obese adults, and is increased after acupuncture. The beneficial effect of acupuncture on obesity is associated with increased plasma nesfatin-1 level.

S-adenosylmethionine-induced adipogenesis is accompanied by suppression of Wnt/ß-catenin and Hedgehog signaling pathways.

S-Adenosylmethionine (SAM) plays a crucial role as a methyl donor in various biological processes and has been previously shown to be involved in adipogenesis in skeletal muscle. This study was conducted to explore the mechanism of SAM inducing adipogenesis in skeletal muscle. Adipose precursor cells, 3T3-L1, and C2C12 cells, were induced into adipogenic differentiation by addition of SAM in MDI-differentiation media (0.5 mmol/L isobutylmethylxanthine, 1 µm/L dexamethasone, and 10 µg/mL insulin) to explore the role of SAM in promoting adipogenesis. Subsequently, cells were cultured with a medium containing SAM alone at the beginning of differentiation to test the relationship between SAM-induced adipogenesis and Wnt/ß-catenin, and Hedgehog signaling pathways that control the cell commitment to adipogenic- or myogenic-differentiation. We found SAM possessed an additive effect with MDI in promoting adipogenesis of 3T3-L1 and C2C12 cells at the beginning of adipogenic differentiation. SAM could also individually induce cell adipogenesis in a dose-dependent manner. Moreover, the expression of Wnt/ß-catenin and Hedgehog signals and their targets were suppressed by SAM (P < 0.05). These results demonstrate that SAM, as an increasingly accepted nutritional supplement, can initiate adipogenesis of adipose precursor cells derived from adipose and muscle tissues, a function at least partly correlated with the suppression of Wnt/ß-catenin and Hedgehog pathways.

Therapeutic properties of quercetin on monosodium urate crystal-induced inflammation in rat.

OBJECTIVES: Gouty arthritis is characterized by intense, acute inflammatory reactions that occur in response to articular deposits of monosodium urate crystals. In this study we have assessed the effects of the flavonoid, quercetin, on monosodium urate crystal-induced inflammation in rats, an experimental model for gouty arthritis. METHODS: Gouty arthritis was induced by intra-articular injection of monosodium urate crystal suspension inside the ankle joint of the rat right hind limb. Circumference was assessed at 2, 4, 8, 12, 24, and 48 h after monosodium urate crystal injection. Histopathological analysis of joint synovial tissue, inflammatory mediator levels, lipid peroxidation, and antioxidant status in serum, liver and joint synovial tissue were determined in control and monosodium urate crystal-treated rats at the end of experiment. KEY FINDINGS: Quercetin treatment attenuated oedema in a dose-dependent manner and decreased histological signs of acute inflammation in the treated animals. In addition, quercetin treatment suppressed leucocyte recruitment, decreased chemokine levels, decreased levels of the lipid peroxidation end-product malondialdehyde, and increased antioxidant enzyme activity in treated rats. CONCLUSIONS: These results indicated that quercetin exerted a strong anti-inflammatory effect that may be useful for the treatment of acute gouty arthritis.

Protective effects of asiaticoside on septic lung injury in mice.

Asiaticoside (AS), a major triterpenoid saponin component isolated from Centella asiatica, has been described to exhibit antioxidant and anti-inflammatory activities. The present study aimed to determine the protective effects and the underlying mechanisms of AS on septic lung injury induced by cecal ligation and puncture (CLP). Mice were pretreated with the AS (45 mg/kg) or AS as well as GW9662 at 1h before CLP, the survival, lung injury, inflammatory mediators and signaling molecules, and Peroxisome proliferator-activated receptor-γ (PPAR-γ) were determined 24 h after CLP. The results showed that AS significantly decreased CLP-induced the mortality, lung pathological damage, the infiltration of mononuclear, polymorphonuclear (PMN) leucocytes and total proteins. Moreover, AS inhibited CLP-induced the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB), the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein in lung tissues, and the production of serum tumor necrosis factor (TNF-α) and interleukin-6 (IL-6). Interestingly, the expression of PPAR-γ protein in lung tissue was up-regulated by AS. Furthermore, GW9662 (the inhibitor of PPAR-γ) significantly reversed these beneficial effects of AS in septic mice. These findings suggest that AS could effectively protect from septic lung injury induced by CLP and the underlying mechanisms might be related to up-regulation of PPAR-γ expression to some extent, which inhibits MAPKs and NF-κB pathway.