ABSTRACT
Small nucleic acid drugs mainly include small interfering RNA(siRNA), antisense oligonucleotide(ASO), microRNA(miRNA), messenger RNA(mRNA), nucleic acid aptamer(aptamer), and so on. Its translation or regulation can be inhibited by binding to the RNA of the target molecule. Due to its strong specificity, persistence, and curability, small nucleic acid drugs have received considerable attention in recent years. Recent studies have shown that some miRNAs from animal and plant sources can stably exist in the blood, tissue, and organs of animals and human beings and exert pharmacological action by regulating the expression of various target proteins. This paper summarized the discovery of small nucleic acids derived from traditional Chinese medicine(TCM) and natural drugs and their cross-border regulatory mechanisms and discussed the technical challenges and regulatory issues brought by this new drug, which can provide new ideas and methods for explaining the complex mechanism of TCM, developing new drugs of small nucleic acids from TCM and natural medicine, and conducting regulatory scientific research.
Subject(s)
Drug Discovery , Drugs, Chinese Herbal , Medicine, Chinese Traditional , Humans , Animals , Drugs, Chinese Herbal/chemistry , Drugs, Chinese Herbal/pharmacology , MicroRNAs/genetics , RNA, Small Interfering/genetics , RNA, Small Interfering/chemistry , Nucleic Acids/chemistryABSTRACT
OBJECTIVE: To examine the anti-inflammatory effects and potential mechanisms of polypeptide from Moschus (PPM) in lipopolysaccharide (LPS)-induced THP-1 macrophages and BALB/c mice. METHODS: The polypeptide was extracted from Moschus and analyzed by high-performance liquid chromatography and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Subsequently, LPS was used to induce inflammation in THP-1 macrophages and BALB/c mice. In LPS-treated or untreated THP-1 macrophages, cell viability was observed by cell counting kit 8 and lactate dehydrogenase release assays; the proinflammatory cytokines and reactive oxygen species (ROS) were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively; and protein and mRNA levels were measured by Western blot and real-time quantitative polymerase chain reaction (qRT-PCR), respectively. In LPS-induced BALB/c mice, the proinflammatory cytokines were measured, and lung histology and cytokines were observed by hematoxylin and eosin (HE) and immunohistochemical (IHC) staining, respectively. RESULTS: The SDS-PAGE results suggested that the molecular weight of purified PPM was in the range of 10-26 kD. In vitro, PPM reduced the production of interleukin 1ß (IL-1ß), IL-18, tumor necrosis factor α (TNF-α), IL-6 and ROS in LPS-induced THP-1 macrophages (P<0.01). Western blot analysis demonstrated that PPM inhibited LPS-induced nuclear factor κB (NF-κB) pathway and thioredoxin interacting protein (TXNIP)/nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3 (NLRP3) inflammasome pathway by reducing protein expression of phospho-NF-κB p65, phospho-inhibitors of NF-κB (Iκ Bs) kinase α/ß (IKKα/ß), TXNIP, NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and pro-caspase-1 (P<0.05 or P<0.01). In addition, qRT-PCR revealed the inhibitory effects of PPM on the mRNA levels of TXNIP, NLRP3, ASC, and caspase-1 (P<0.05 or P<0.01). Furthermore, in LPS-induced BALB/c mice, PPM reduced TNF-α and IL-6 levels in serum (P<0.05 or P<0.01), decreased IL-1ß and IL-18 levels in the lungs (P<0.01) and alleviated pathological injury to the lungs. CONCLUSION: PPM could attenuate LPS-induced inflammation by inhibiting the NF-κB-ROS/NLRP3 pathway, and may be a novel potential candidate drug for treating inflammation and inflammation-related diseases.
ABSTRACT
Yi Yin, a famous medical scientist and culinary master in the late Xia Dynasty and early Shang Dynasty, developed the Chinese medicinal liquids and Chinese medicinal prescriptions emerged after that. Chinese medicinal prescriptions have attracted much attention because of their unique advantages in the treatment of chronic multifactorial diseases, representing an important direction of drug discovery in the future. Yiyin decoction theory is the superior form of personalized combined medication with advanced consciousness. It is different from not only the magic bullet theory of single component action but also the connotation of modern multi-target drugs. The core of Yiyin decoction theory can be summarized as compound compatibility, multiple effects, and moderate regulation. Compound compatibility refers to that the formulation of Chinese medicinal prescriptions involves the complex synergy and interactions between sovereign, minister, assistant, and guide medicinal materials. Multiple effects mean that the prescriptions employ a variety of mechanisms to exert comprehensive pharmacological effects of nonlinear feedback. Moderate regulation reflects that the prescriptions can accurately regulate the multiple points of the disease biological network as a whole. To solve the mystery of Yiyin decoction theory, we should not only simply study the known active substances(components) and their independent target effects in the mixture, but also mine the "dark matter" and "dark effect" of Chinese medicinal prescriptions. That is, we should learn the neglected atypical pharmacological effects of Chinese medicinal prescriptions and the multi-point nesting mechanism that plays a precise regulatory function in the body. Yiyin decoction theory focuses on the overall pharmacological effect to reflect the comprehensive clinical value of Chinese medicinal prescriptions, which is of great significance for the development of a new model for the evaluation and application of new Chinese medicinal prescriptions in line with the theory of traditional Chinese medicine.
Subject(s)
Drugs, Chinese Herbal , China , Drugs, Chinese Herbal/pharmacology , Medicine, Chinese Traditional , PrescriptionsABSTRACT
Excessive reactive oxygen species (ROS) accumulation is involved in the pathogenesis of liver fibrosis and damage, specifically in the developing embryo that is extremely sensitive to oxidative stress. Herein, a liver injury model in chick embryo was established by using 2,2-azobis (2-amidinopropane) dihydrochloride (AAPH), which was used to investigate the effect of cyclo(-Phe-Phe) (CPP), a natural dipeptide found in foods and beverages. The results showed that CPP significantly alleviated AAPH-induced liver pathological damage, hepatic dysfunction and inhibited the excessive production of ROS in both chick embryo liver and HepG2 cells. Additionally, CPP increased the antioxidative activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD), as well as elevated the level of glutathione (GSH), suggesting that CPP combating liver injury probably depends on its antioxidant capability. Mechanistically, CPP upregulated the mRNA and protein expression of heme oxyense-1 (HO-1) and NADPH quinone oxidoreductase 1 (NQO1) in vivo and in vitro, along with promoting the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) while inhibiting its degradation through binding with Kelch-like ECH-associated protein 1 (Keap1). In conclusion, this study proposes a potential peptide drug for the treatment of hepatic damage induced by oxidative stress and also unravels its mechanism of action.
Subject(s)
Dipeptides , NF-E2-Related Factor 2 , Animals , Chick Embryo , Antioxidants/metabolism , Dipeptides/pharmacology , Glutathione/metabolism , Kelch-Like ECH-Associated Protein 1/metabolism , Liver/metabolism , NF-E2-Related Factor 2/genetics , NF-E2-Related Factor 2/metabolism , Oxidative Stress , Reactive Oxygen Species/metabolismABSTRACT
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
ABSTRACT
For the basic research on the traditional Chinese medicine(TCM), objective syndrome of traditional Chinese medicine and evaluation criteria of traditional Chinese medicine compounds are hardly to break though. While, the modern immunology points out that the body is a counterbalance state and immune imbalance is the root of sickness. The thinking mode of treating diseases in traditional Chinese medicine is also "balance", considering disease is the result of bias which present the imbalance of "Yin counters Yang", "exterior counters interior", "cold counters heat" and "weak counters strong". The Chinese herbal compound formula preparation was applied on disease therapy based on theory of Chinese medicine, which was confirmed by long period clinical application. It is composed of multi-compounds and has the characteristic of multi-targeting. Integrative medicine has spawned pan-immunomics, and the evaluation of immune function (immune balance) has become an important basis for diagnosis and treatment models of integrative medicine. In addition, balance is the core idea of whole-systemic conception of traditional Chinese medicine. Therefore, we speculate that immune balance under pan-immunomic can bridge the traditional Chinese medicine and modern integrative medicine and is the important basis for objective syndrome of traditional Chinese medicine and evaluation criteria of traditional Chinese medicine compounds. According to the bridging theory, we attempt to utilize informatics and statistical methods to construct an evaluation system for pharmacodynamics of traditional Chinese medicine based on its moderate regulation and the balanced adjustment of immunity under pan-immunomic, which further reveal the scientific essence of the whole-systemic view of traditional Chinese medicine. This research brings out a new valuable strategy and provides a theoretical basis for accelerating the transformation of traditional Chinese medicine, especially the exploitation of Chinese herbal compound formula, and constructing the new drug innovation and review system for traditional Chinese medicine. Besides as a reference for traditional Chinese medicine objective syndrome and pharmacodynamics of traditional Chinese medicine compounds, the evaluation system can screen the immunity of sub-health population also. With the continuous accumulation of clinical sample and data, the evaluation system will be more accurate and intelligent.
Subject(s)
Drugs, Chinese Herbal/pharmacology , Immune System/drug effects , Medicine, Chinese Traditional , Humans , Syndrome , Yin-YangABSTRACT
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder and there is no effective cure for this devastating disease to date. Bushen Yizhi Formula (BSYZ-F), a Chinese herbal compound, has proved to be effective for AD. In this study, we further investigate the effective part of BSYZ-F, ethyl acetate extract components of BSYZ-F (BSYZ-E), protects scopolamine (SCOP)-induced cognitive impairment, which shows a similar effect to BSYZ-F. We also find that BSYZ-E could protect against SCOP-induced cholinergic system dysfunction. In neuron function level, BSYZ-E remarkably elevates protein levels of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). BSYZ-E also significantly mitigates SCOP-induced apoptosis, oxidative stress and nitrosative stress. Conclusively, BSYZ-E, the effective part of BSYZ-F, can provide neuroprotection against SCOP-induced cognitive impairment through a multifunctional strategy. These findings suggest that BSYZ-E might be developed as a therapeutic drug for AD by targeting multiple pathways of the pathogenesis.
Subject(s)
Cognitive Dysfunction/etiology , Cognitive Dysfunction/psychology , Drugs, Chinese Herbal/pharmacology , Neuroprotective Agents/pharmacology , Scopolamine/adverse effects , Animals , Apoptosis/drug effects , Biomarkers , Brain/drug effects , Brain/metabolism , Cognitive Dysfunction/drug therapy , Cognitive Dysfunction/metabolism , Disease Models, Animal , Drugs, Chinese Herbal/chemistry , Immunohistochemistry , Maze Learning/drug effects , Memory/drug effects , Mice , Neurons/drug effects , Neurons/metabolism , Neuroprotective Agents/chemistry , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II/metabolism , Oxidative Stress/drug effectsABSTRACT
Neural tube defects (NTDs) are among the most common of the embryonic abnormalities associated with hyperglycemic gestation. In this study, the molecular mechanisms of embryonic neurogenesis influenced by hyperglycemia was investigated using chicken embryo models. High-concentration glucose was administered into chicken eggs and resulted in increased plasma and brain tissue glucose, and suppressed expression of glucose transporters (GLUTs). The rate of NTD positively correlated with hyperglycemia. Furthermore, abnormally increased O-GlcNAcylation, a nutritionally responsive modification, of the key neural tube marker Pax3 protein led to the loss of this protein. This loss was not observed in a folate-deficiency NTD induced by methotrexate. Carnosine, an endogenous dipeptide, showed significant recovery effects on neural tube development. In contrast, folic acid, a well-known periconceptional agent, surprisingly showed relatively minimal effect. Higher expression levels of the Pax3 protein were found in the carnosine-treated groups, while lower expression levels were found in folic acid groups. Furthermore, the abnormal O-GlcNAcylation of the Pax3 protein was restored by carnosine. These results suggest new insights into using endogenous nutrients for the protection of embryonic neurodevelopment affected by diabetes gestation. The abnormal excessive O-GlcNAcylation of Pax3 may be responsible for the neural tube defects associated with hyperglycemia.
Subject(s)
Carnosine/therapeutic use , Folic Acid/therapeutic use , Glucose/toxicity , Hyperglycemia/metabolism , Neural Tube Defects/metabolism , PAX3 Transcription Factor/metabolism , Acylation/drug effects , Acylation/physiology , Animals , Carnosine/pharmacology , Chick Embryo , Dose-Response Relationship, Drug , Folic Acid/pharmacology , Hyperglycemia/chemically induced , Hyperglycemia/drug therapy , Neural Tube Defects/chemically induced , Neural Tube Defects/drug therapyABSTRACT
Gestational diabetes mellitus (GDM) is one of the leading causes of fetal malformations. However, few models have been developed to study the underlying mechanisms of GDM-induced fetal eye malformation. In this study, a high concentration of glucose (0.2â mmol per egg) was injected into the air sac of chick embryos on embryo development day (EDD) 1 to develop a hyperglycemia model. Results showed that 47.3% of embryonic eye malformation happened on EDD 5. In this model, the key genes regulating eye development, Pax6, Six3 and Otx2, were downregulated by hyperglycemia. Among these genes, the expression of Pax6 was the most vulnerable to hyperglycemia, being suppressed by 70%. A reduction in Pax6 gene expression induced eye malformation in chick embryos. However, increased expression of Pax6 in chick embryos could rescue hyperglycemia-induced eye malformation. Hyperglycemia stimulated O-linked N-acetylglucosaminylation, which caused oxidative stress in chick embryos. Pax6 was found to be vulnerable to free radicals, but the antioxidant edaravone could restore Pax6 expression and reverse eye malformation. These results illustrated a successful establishment of a new chick embryo model to study the molecular mechanism of hyperglycemia-induced eye malformation. The suppression of the Pax6 gene is probably mediated by oxidative stress and could be a crucial target for the therapy of GDM-induced embryonic eye malformation.
Subject(s)
Diabetes, Gestational/metabolism , Disease Models, Animal , Eye Abnormalities/genetics , Eye Proteins/genetics , Homeodomain Proteins/genetics , Paired Box Transcription Factors/genetics , Repressor Proteins/genetics , Animals , Chick Embryo , Female , Hyperglycemia/genetics , Oxidative Stress , PAX6 Transcription Factor , Plasmids , PregnancyABSTRACT
Gestational diabetes mellitus (GDM) is one of the leading causes of offspring malformations, in which eye malformation is an important disease. It has raised demand for therapy to improve fetal outcomes. In this study, we used chick embryo to establish a GDM model to study the protective effects of proanthocyanidins on eye development. Chick embryos were exposed to high glucose (0.2 mmol/egg) on embryo development day (EDD) 1. Proanthocyanidins (1 and 10 nmol/egg) were injected into the air sac on EDD 0. Results showed that both dosages of proanthocyanidins could prevent the eye malformation and rescue the high glucose-induced oxidative stress significantly, which the similar effects were showed in edaravone. However, proanthocyanidins could not decrease the glucose concentration of embryo eye. Moreover, the key genes regulating eye development, Pax6, was down-regulated by high glucose. Proanthocyanidins could restore the suppressed expression of Pax6. These results indicated proanthocyanidins might be a promising natural agent to prevent high glucose-induced eye malformation by restoring Pax6 expression.
Subject(s)
Eye Proteins/genetics , Eye/drug effects , Gene Expression Regulation, Developmental/drug effects , Glucose/adverse effects , Homeodomain Proteins/genetics , Paired Box Transcription Factors/genetics , Proanthocyanidins/pharmacology , Repressor Proteins/genetics , Animals , Chick Embryo , Down-Regulation , Embryonic Development , Eye/embryology , Eye Proteins/metabolism , Homeodomain Proteins/metabolism , Organogenesis/drug effects , PAX6 Transcription Factor , Paired Box Transcription Factors/metabolism , Reactive Oxygen Species/metabolism , Repressor Proteins/metabolismABSTRACT
Resveratrol, a famous plant-derived polyphenolic phytoalexin, has been considered to play physiological roles such as antioxidative, neuroprotective, and anticancer effects in adults. However, its antioxidative activity and neuroprotective effect were seldom discussed in the embryonic system. In this study, the effect of resveratrol on chicken embryo development under high glucose and its underlying mechanism of resveratrol were investigated. High glucose administrated to chicken embryo at embryonic Day 1 induced stillbirth, growth retardation, and impaired blood vessel development on yolk sac. However, resveratrol supplementation before glucose exposure showed significant effect on decreasing the death rate, developmental damage, and vessel injury. In addition, oxidative stress was caused by high-glucose exposure, and resveratrol could rescue this high-glucose-induced oxidative stress. Moreover, the neural developmental marker paired box 3 was significantly decreased by high glucose and recovered by resveratrol. Cell cycle-regulated gene expression was also intervened by resveratrol. This study had found an association between resveratrol and hyperglycemia-induced embryonic damage, which suggested a potential protective effect of resveratrol on gestational diabetes.
Subject(s)
Glucose/toxicity , Neuroprotective Agents/pharmacology , Stilbenes/pharmacology , Animals , Biological Products/pharmacology , Chickens , Glucose/analysis , Molecular Structure , Reactive Oxygen Species/metabolism , Resveratrol , Stilbenes/chemistryABSTRACT
The beneficial effect of caffeine-containing food on non-alcoholic fatty liver disease (NAFLD) has been widely reported. The aim of this study was to explore the effect of caffeine on hepatic steatosis. C57BL/6 mice were randomly assigned to a normal diet or a high energy diet (HED). Caffeine was given to HED mice by oral gavage. Body weights, lipids in the liver and liver damage were measured. Meanwhile, cAMP, SIRT3 or AMPK inhibitors were treated respectively before incubation with caffeine in oleate-treated HepG2 cells. SIRT3 was further silenced by siRNA to confirm the results. Caffeine significantly decreased the mass of fat tissues, lipids, ALT and AST levels in the liver of HED-treated mice. Caffeine increased the transformation of ADP to ATP and activated the cAMP/CREB/SIRT3/AMPK/ACC pathway in the liver. Nile red staining demonstrated that suppression of cAMP, SIRT3 or AMPK in oleate-treated HepG2 cells counteracted the effect of caffeine. Moreover, knocking down SIRT3 could down-regulate AMPK and ACC phosphorylation by caffeine. These results demonstrate that caffeine could improve HED-induced hepatic steatosis by promoting lipid metabolism via the cAMP/CREB/SIRT3/AMPK/ACC pathway. SIRT3 functioned as a molecular bridge connecting caffeine and lipid metabolism.
Subject(s)
Caffeine/administration & dosage , Lipid Metabolism , Non-alcoholic Fatty Liver Disease/drug therapy , Sirtuin 3/metabolism , AMP-Activated Protein Kinases/genetics , AMP-Activated Protein Kinases/metabolism , Acetyl-CoA Carboxylase/genetics , Acetyl-CoA Carboxylase/metabolism , Animals , CREB-Binding Protein/genetics , CREB-Binding Protein/metabolism , Diet, High-Fat/adverse effects , Humans , Liver/drug effects , Liver/enzymology , Liver/metabolism , Male , Mice , Mice, Inbred C57BL , Non-alcoholic Fatty Liver Disease/enzymology , Non-alcoholic Fatty Liver Disease/genetics , Non-alcoholic Fatty Liver Disease/metabolism , Sirtuin 3/geneticsABSTRACT
It is well known that vitamin C could protect against influenza infection, but little is known about the mechanisms. This study aimed to investigate the influence and possible mechanisms of vitamin C on pneumonia induced by influenza virus in stressed mice. Results showed that restraint stress significantly increased the mortality and the severity of pneumonia in mice caused by A/FM/1/47(H1N1) virus infection, which was attenuated by oral administration of vitamin C (125 and 250 mg/kg). Moreover, vitamin C administration significantly decreased expression of susceptibility genes, including mitochondrial antiviral signaling (MAVS) and interferon regulatory factor 3 (IRF3), and increased expression of NF-κB. These work in conjunction to induce type I interferons (IFNs) and elicit innate antiviral response as key factors in RIG-I-mediated signal transduction pathway. The above effects of vitamin C were further found to relate with inhibition of excess CORT synthesis by regulating steroid hydroxylating enzymes in adrenal gland. In conclusion, the protective effects of vitamin C on influenza virus-caused pneumonia might be related to its inhibition of CORT synthesis, which reduces the susceptibility to influenza viral infection in restraint-stressed mice. These findings provide a new mechanism for the effects of vitamin C on influenza virus-induced pneumonia in restraint-stressed mice.
Subject(s)
Ascorbic Acid/administration & dosage , Influenza A Virus, H1N1 Subtype , Influenza, Human/drug therapy , Influenza, Human/immunology , Pneumonia, Viral/drug therapy , Pneumonia, Viral/immunology , Animals , Humans , Male , Mice , Reactive Oxygen Species/immunology , Restraint, Physical , Stress, Physiological/drug effects , Stress, Physiological/immunology , Treatment OutcomeABSTRACT
The most commonly applied strategies for the evaluation of antioxidant capacity are the chemical- or cell-based approaches. However, the results obtained from these methods might not reflect the antioxidant ability of test samples within organisms. In this study, we propose a combination of experiments, including oxygen radical absorbance capacity (ORAC), cellular antioxidant activity assay (CAA), and the chick embryo model, as an efficient trio to evaluate antioxidant capacity of food components. Taking purine alkaloids as example, results demonstrate that chemical and cellular method might misinterpret their true ability on antioxidation. In chick embryo model, caffeine and theacrine can significantly improve vessel density on chorioallantoic membrane and myocardial apoptosis. The mechanism can be involving multiple targets within the organism. We believe that the trio proposed can be widely utilized in screening massive number of antioxidant in a cost-effective way. It will also help discovering new antioxidants that are easily being omitted due to their relatively poor in vitro activities.
Subject(s)
Antioxidants/chemistry , In Vitro Techniques/methods , Purines/chemistry , Alkaloids , Animals , Caffeine , Chick Embryo , Oxidation-ReductionABSTRACT
Prenatal exposure to ethanol has been reported to cause developmental defects in the brain. During brain development, a sufficient energy source is deemed essential and glucose is regarded as the primary energy source for neurons. In this study, the impact of ethanol on embryonic malformation and cerebral glucose metabolism in developing embryo was investigated. Different doses of ethanol (0, 10, 20, 40 mg/egg) were administrated to chicken embryos after 36 h incubation. Embryonic brain weight was found significantly decreased. Moreover, we observed an obvious reduction of neurofilament expression in the central nervous system (CNS) by immunostaining assay. All the above indicated that ethanol exposure caused obvious CNS damages and resulted malformations in the developing brain. Mechanism research showed that cerebral glucose and lactic acid contents, activities of hexokinase, pyruvate kinase and lactic dehydrogenase were decreased dose dependently. Meanwhile, mRNA levels of glucose transporter 1, glucose transporter 3 and insulin-like growth factor I in the brain demonstrated a significant decrease in gene expression after ethanol exposure. These results suggested that glucose metabolism disorder is an important risk factor in ethanol exposure induced malformation in embryonic brain.
Subject(s)
Brain/embryology , Ethanol/adverse effects , Glucose Metabolism Disorders/embryology , Animals , Brain/drug effects , Brain/pathology , Chick Embryo , Ethanol/administration & dosage , Gene Expression Regulation/drug effects , Glucose/metabolism , Glucose Metabolism Disorders/chemically induced , Glucose Metabolism Disorders/pathology , Glucose Transporter Type 1/genetics , Glucose Transporter Type 1/metabolism , Glucose Transporter Type 3/genetics , Glucose Transporter Type 3/metabolism , Hexokinase/metabolism , Insulin-Like Growth Factor I/genetics , Insulin-Like Growth Factor I/metabolism , Lactic Acid/metabolism , Neurons/drug effects , Neurons/pathology , Organ Size/drug effects , Pyruvate Kinase/metabolism , Risk FactorsABSTRACT
Sarcandra glabra, as a type of "antipyretic-detoxicate drugs", has always been widely used in traditional Chinese medicine (TCM). The Sarcandra glabra extract (SGE) is applied frequently as anti-inflammatory and anti-infectious drug in folk medicine. However, relative experiment data supporting this effective clinical consequence was limited. In order to mimic the physiological conditions of the susceptible population, we employed restraint stress mouse model to investigate the effect of SGE against influenza. Mice were infected with influenza virus three days after restraint, while SGE was orally administrated for 10 consecutive days. Body weight, morbidity, and mortality were recorded daily. Histopathologic changes, susceptibility genes expressions and inflammatory markers in lungs were determined. Our results showed that restraint stress significantly increased susceptibility and severity of influenza virus. However, oral administration of SGE could reduce morbidity, mortality and significantly prolonged survival time. The results further showed that SGE had a crucial effect on improving susceptibility markers levels to recover the balance of host defense system and inhibiting inflammatory cytokines levels through down-regulation of NF-κB protein expression to ameliorate the lung injury. These data showed that SGE reduced the susceptibility and severity of influenza.