Dachengqi decoction alleviates acute lung injury by suppressing HIF-1α-mediated glycolysis.

ETHNOPHARMACOLOGICAL RELEVANCE: Acute lung injury (ALI) is an aggressive inflammatory disease of the lungs characterized by a high mortality rate. More and more researchers have found that herbal medicines are highly effective in preventing and treating inflammatory lung diseases. Among them, Dachengqi Decoction (DCQD) is considered to be the representative prescription of "lung-intestine combined treatment" in traditional Chinese medicine, and its potential protective mechanism against ALI is worthy of further study. AIM OF THE STUDY: Based on the theory of "lung-intestine combined treatment", the protective effect and molecular mechanism of DCQD in alleviating ALI were verified by network pharmacology and experiments. MATERIALS AND METHODS: The active ingredients of DCQD were obtained by UPLC-MS. Network pharmacology and molecular docking techniques were used to screen the active ingredient-target pathway of DCQD for ALI treatment. Additionally, the ALI model was constructed and verified in vivo according to the predicted results. RESULTS: 34 active components and 570 potential targets of DCQD were selected by network pharmacological analysis. In addition, 950 target genes of ALI and 2095 target genes related to sepsis were obtained, and 570 interlinked target genes of the two were identified. We finally screened out 199 common target genes critical to DCQD treatment of ALI and sepsis, and then enriched them with GO and KEGG. In the ALI model, studies have found that DCQD alleviates the inflammatory response of ALI, possibly by inhibiting HIF-1α-mediated glycolysis. CONCLUSION: This study confirmed the preventive effect of DCQD on ALI, and found that DCQD can improve the protective mechanism of ALI by regulating the expression of HIF-1α, down-regulating glycolysis and reducing inflammation.

Herba Patriniae and its component Isovitexin show anti-colorectal cancer effects by inducing apoptosis and cell-cycle arrest via p53 activation.

Colorectal cancer (CRC) is the most prevalent cancer of the digestive tract. Herba Patriniae (also known as Bai Jiang Cao, HP) have been widely used to manage diarrhea, ulcerative colitis, and several cancers, including CRC. Nonetheless, the molecular mechanisms underlying the pharmacological action of HP on CRC remain unclear. This study investigated the underlying mechanisms of HP against CRC using network pharmacology analysis and in vitro and in vivo experiments. The results revealed nine bioactive compounds of HP. Furthermore, 3460 CRC-related targets of the identified active compounds were predicted from the Gene Expression Omnibus (GEO) database. Furthermore, 65 common targets were identified through the intersection of two related targets. Moreover, ten hub genes, including CDK4, CDK2, CDK1, CCND1, CCNB1, CCNA2, MYC, E2F1, CHEK1, and CDKN1A were identified through the topological analysis. Meanwhile, the GO and KEGG pathway analysis revealed that the core target genes were majorly enriched in the p53 and HIF-1 signaling pathways. Moreover, HP promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway in a dose-dependent manner, while a similar effect was observed for Isovitexin (the primary component of HP). Overall, this study provides valuable insights into the underlying mechanisms of HP and its component Isovitexin against CRC, providing a theoretical foundation for additional experimental verification of its clinical application.

Effects of Bacillus licheniformis on the Growth Performance, Antioxidant Capacity, Ileal Morphology, Intestinal Short Chain Fatty Acids, and Colonic Microflora in Piglets Challenged with Lipopolysaccharide.

The aim of the present study was to investigate the effects of Bacillus licheniformis (BL) on the growth performance, antioxidant capacity, ileal morphology, intestinal fecal short-chain fatty acids, and microflora of weaned piglets challenged with lipopolysaccharide (LPS). Piglets were assigned into three groups: basal diet (Con), a basal diet with added 109 CFU B. licheniformis/kg (BLl), and a basal diet with added 1010 CFU B. licheniformis/kg (BLh). On day 28, BLh piglets were intraperitoneally injected with LPS (CBL) and sterilized saline water (BL), Con piglets were injected with LPS (LPS) and sterilized saline water (Con), with the injections being administered for three consecutive days. The average daily gain significantly increased from day 1 to day 28 and the feed: gain ratio decreased with BL supplementation compared with the Con group. Supplementation with BLl and BLh reduced the diarrhea rate in piglets. Serum catalase activity increased and malondialdehyde concentration decreased in the CBL treatment group compared with the LPS treatment group. Both BL and CBL treatments increased the ileal villus length/crypt depth ratio compared with Con and LPS treatments. BL administration significantly increased colonic propionic and isobutyric acid concentrations compared with Con treatment. Both BL and CBL piglets had significantly increased fecal acetic, propionic, and butyric acid levels compared with LPS piglets. Analysis of the colonic microbial metagenome showed that Prevotella species were the predominant bacteria in piglets treated with BL and CBL. The CBL-treated piglets had higher scores for lysine biosynthesis, arginine biosynthesis, sulfur relay system, and histidine metabolism. BL-treated piglets had higher scores for glycosaminoglycan biosynthesis-keratan sulfate, oxidative phosphorylation, and pyruvate and carbon metabolism.

Oridonin promotes endoplasmic reticulum stress via TP53-repressed TCF4 transactivation in colorectal cancer.

BACKGROUND: The incidence of colorectal cancer and cancer death rate are increasing every year, and the affected population is becoming younger. Traditional Chinese medicine therapy has a unique effect in prolonging survival time and improving the prognosis of patients with colorectal cancer. Oridonin has been reported to have anti-cancer effects in a variety of tumors, but the exact mechanism remains to be investigated. METHODS: Cell Counting Kit-8 assay (CCK8) and 5-Ethynyl-2'-deoxyuridine (EdU) staining assay, Tranwell, and Wound healing assays were performed to measure cell proliferation, invasion, and migration capacities, respectively. The protein and mRNA expression levels of various molecules were reflected by Western blot and Reverse Transcription quantitative Polymerase Chain Reaction (qRT-PCR). Transcription Factor 4 (TCF4) and its target genes were analyzed by Position Weight Matrices (PWMs) software and the Gene Expression Omnibus (GEO) database. Immunofluorescence (IF) was performed to visualize the expression and position of Endoplasmic Reticulum (ER) stress biomarkers. The morphology of the ER was demonstrated by the ER tracker-red. Reactive Oxygen Species (ROS) levels were measured using a flow cytometer (FCM) or fluorescent staining. Calcium ion (Ca2+) concentration was quantified by Fluo-3 AM staining. Athymic nude mice were modeled with subcutaneous xenografts. RESULTS: Oridonin inhibited the proliferation, invasion, and migration of colorectal cancer, and this effect was weakened in a concentration-dependent manner by ER stress inhibitors. In addition, oridonin-induced colorectal tumor cells showed increased expression of ER stress biomarkers, loose morphology of ER, increased vesicles, and irregular shape. TCF4 was identified as a regulator of ER stress by PWMs software and GEO survival analysis. In vitro and in vivo experiments confirmed that TCF4 inhibited ER stress, reduced ROS production, and maintained Ca2+ homeostasis. In addition, oridonin also activated TP53 and inhibited TCF4 transactivation, further exacerbating the elevated ROS levels and calcium ion release in tumor cells and inhibiting tumorigenesis in colorectal cancer cells in vivo. CONCLUSIONS: Oridonin upregulated TP53, inhibited TCF4 transactivation, and induced ER stress dysregulation in tumor cells, promoting colorectal cancer cell death. Therefore, TCF4 may be one of the important nodes for tumor cells to regulate ER stress and maintain protein synthesis homeostasis. And the inhibition of the TP53/TCF4 axis plays a key role in the anti-cancer effects of oridonin.

Vitamin B12 alleviates myocardial ischemia/reperfusion injury via the SIRT3/AMPK signaling pathway.

AIM: To examine the protective effect of vitamin B12 against myocardial ischemia/reperfusion (I/R) injury and elucidate its underlying mechanism of action. METHODS: Mice were subjected to myocardial I/R injury by left anterior descending coronary artery (LAD) occlusion followed by 24 h reperfusion. Cardiac function and injury were evaluated by echocardiography, triphenyl tetrazolium chloride (TTC) and cardiac troponin T (cTnT) staining, and measuring lactate dehydrogenase (LDH) levels. In addition, various molecular and biochemical methods, as well as RNA sequencing were used to determine the effects and mechanism of action of vitamin B12 on I/R injury. RESULTS: We found that high doses of vitamin B12 inhibited myocardial I/R injury. Furthermore, our data indicated that vitamin B12 supplementation alleviated cardiac dysfunction and injury by mitigating oxidative stress and apoptosis through downregulation of Nox2, the Ac-SOD2/SOD2 and Bax/Bcl-2 ratios and cleaved caspase-3 expression, and upregulation of SIRT3 expression and AMPK activity. However, these effects were largely reversed following treatment with the SIRT3 inhibitor, 3-TYP. Our RNA-sequencing data further demonstrated that vitamin B12 supplementation reduced inflammation during I/R injury. CONCLUSION: High doses of vitamin B12 supplements improved myocardial I/R injury by suppressing the accumulation of reactive oxygen species and apoptosis of myocardial tissue through modulation of the SIRT3/AMPK signaling pathway, while reducing inflammation. Our findings suggested that vitamin B12 administered at high doses could be a potential therapy for myocardial I/R damage.

Mechanism of Sijunzi Decoction in the treatment of colorectal cancer based on network pharmacology and experimental validation.

ETHNOPHARMACOLOGICAL RELEVANCE: Sijunzi Decoction（SJZD）, as a famous classical prescription for the treatment of colorectal cancer(CRC) in the traditional Chinese medicine (TCM), has achieved good curative effects in clinical practice. However, its specific ingredients and molecular mechanisms is still unclear. AIM OF THE STUDY: To analyze the effective ingredients and molecular mechanisms of SJZD in the treatment of CRC through network pharmacology technology and experimental validation. MATERIALS AND METHODS: First, the TCM Systems Pharmacology database and analysis platform database were searched to screen the effective chemical components of SJZD. Swiss Target Prediction was used to predict corresponding potential target genes of compounds. After that, we constructed a components and corresponding target network by Cytoscape. Simultaneously, 5 disease databases were used to search and filter CRC targets, and then we constructed a drug-disease target protein-protein interaction (PPI) network. Cytoscape 3.7 was used for visualization and cluster analysis, and Metascape database was used for GO and KEGG enrichment analysis. We drew the main pathway-target network diagram. Autodock vina1.5.6 was applied to molecular docking for the main compounds and target proteins. Subsequently, the potential mechanism of SJZD on colon cancer predicted by network pharmacological analysis was experimentally studied and verified in vivo and in vitro. RESULTS: 144 effective active chemical components, 897 potential targets, and 2584 CRC target genes were screened out. The number of common targets between the SJZD and CRC was 414.3250 GO biological process items and 186 KEGG signal pathways were obtained after analysis. The main compounds and the target protein had a good binding ability in molecular docking. The results of cell and animal experiments showed that SJZD could promote apoptosis and autophagy of CRC cells through PI3K/Akt/mTOR pathway. CONCLUSIONS: SJZD can treat CRC through multiple components, multiple targets and multiple pathways. We initially revealed the effective components and molecular mechanisms of SJZD in the treatment of CRC, and we used molecular docking and experiment for preliminary verification.

Integrated network pharmacology and experimental verification to investigate the mechanisms of YYFZBJS against colorectal cancer via CDK1/PI3K/Akt signaling.

Background: Colorectal cancer (CRC) is a common digestive tract malignancy with rising incidence and morbidity worldwide during recent years. Yi-Yi-Fu-Zi-Bai-Jiang-San (YYFZBJS), a traditional Chinese medicine formula, has showed positive effects against cancers. However, the mechanisms underlying its anticancer effects requires investigation. Methods: Information on bioactive compounds, potential YYFZBJS targets, and CRC-associated genes, was obtained from public databases. The key targets and ingredients as well their corresponding signaling pathways were identified using bioinformatic approaches, including Kyoto encyclopedia of genes and genomes (KEGG) analyses, gene ontology (GO), and protein-protein interaction (PPI). Subsequently, molecular docking was used to verify the main compounds-targets. Potential YYFZBJS therapeutic effects against CRC were validated in vitro and in vivo. Results: Using pharmacological network analysis, 40 YYFZBJS active compounds and 21 potential anti-CRC targets were identified. YYFZBJS was an important regulator of CRC through various targets and signaling pathways, particularly the cell cycle and PI3K/AKT pathway. Additionally, YYFZBJS suppressed the proliferation of CRC cells. Flow cytometry showed that YYFZBJS induced apoptosis and cell cycle arrest in the G2/M phase. Western blotting analysis indicated that YYFZBJS reduced the protein levels of CDK1, p-AKT, and p-PI3K, without altering total PI3K and AKT protein levels. In vivo analysis found that YYFZBJS inhibited tumor growth and PI3K/AKT signaling in a mouse model of CRC. Conclusion: As predicted by network pharmacology and validated by the experimental results, YYFZBJS inhibited proliferation, induced apoptosis and arrested cell cycle progression in CRC by modulating the CDK1/PI3K/Akt signaling pathway.

Emodin Attenuates LPS-Induced Acute Lung Injury by Inhibiting NLRP3 Inflammasome-Dependent Pyroptosis Signaling Pathway In vitro and In vivo.

Emodin, the effective component of the traditional Chinese medicine Dahuang, has anti-inflammatory effects. However, the protective effects and potential mechanisms of emodin are not clear. This study investigated the protective effects and potential mechanisms of emodin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in vitro and in vivo. In vivo, we designed an LPS-induced ALI rat model. In vitro, we chose the J774A.1 cell line to establish an inflammatory cellular model, and knocked down NOD-like receptor family pyrin domain containing 3 (NLRP3) using small interfering RNA. The mRNA and protein expression of NLRP3, a C-terminal caspase recruitment domain (ASC), caspase 1 (CASP1), and gasdermin D (GSDMD) in cells and lung tissues were detected by western blot and real-time quantitative polymerase chain reaction (PCR). The expression levels of interleukin 1 beta (IL-1ß) and IL-18 in the serum and supernatant were determined by the enzyme-linked immunosorbent assay. The degree of pathological injury in lung tissue was evaluated by hematoxylin and eosin (H&E) staining. In vitro, we demonstrated that emodin could inhibit NLRP3 and then inhibit the expression of ASC, CASP1, GSDMD, IL-1ß, and IL-18. In vivo, we confirmed that emodin had protective effects on LPS-induced ALI and inhibitory effects on NLRP3 inflammasome -dependent pyroptosis. Emodin showed excellent protective effects against LPS-induced ALI by regulating the NLRP3 inflammasome-dependent pyroptosis signaling pathway.

Chinese herbal preparations for chronic heart failure: Study protocol for an umbrella review of systematic reviews and meta-analyses.

BACKGROUND: Chinese herbal preparations (CHPs) have been reported to be effective in the management of chronic heart failure (CHF); they are beneficial in improving cardiac function, reducing hospital stays and readmission. However, the credibility of their effectiveness evidence has not been evaluated. We aim to summarize and evaluate current effectiveness evidence of traditional Chinese medicine in the management of CHF. METHODS: We will search PubMed, Embase, the Cochrane Database of Systemic Review (CDSR), and Web of Science from inception to December 2019 for systematic reviews that assessing the effectiveness of CHPs for CHF. The search will be performed without language restriction. Experimental interventions will include any type of CHPs, and control interventions will include placebo, sham interventions, usual care, or no controls. The primary outcome will be the changes in heart function classification defined by the New York Heart Association. Secondary outcomes include left ventricular ejection fraction, Six Minute Walk Test, other efficacy outcomes, and adverse events. We will use I statistics to assess the between-study heterogeneity in each meta-analysis, Eager test to detect publication bias, and the ratio of observed versus expected number of trials with positive findings. We will summarize the evidence and classify them into convincing, highly suggestive, suggestive, or weak. RESULTS: The results of this study will be published in a peer-reviewed journal. ETHICS AND DISSEMINATION: No ethical approval and patient consent are required since this study data is based on published literature. The results of the study will be submitted to a peer-reviewed journal. PROTOCOL REGISTRATION NUMBER: PROSPERO CRD 42019139649 (https://www.crd.york.ac.uk/PROSPERO/#joinuppage).

Effect of Quyu Chencuo Formula () on Renal Fibrosis in Obstructive Nephropathy Rats.

OBJECTIVE: To observe the effect of Quyu Chencuo Formula (, QCF) on renal fibrosis in rats with obstructive nephropathy. METHODS: Twenty-four rats were randomly divided into three groups, 4 for sham operation as the control group, 10 for unilateral ureteral obstruction (UUO) model group, and the rest 10 for QCF treating UUO model group. All rats were sacrificed under 3% pentobarbital (50 mg/kg) anesthesia on the 14th day after surgery, then the right kidney samples of rats were harvested for hematoxylin eosin (HE) staining and Masson staining to observe the renal pathological changes. Immunohistochemistry and Western blotting were used to examine the expression of transforming growth factor ß1 (TGF-ß1), and real-time polymerase chain reaction (RT-PCR) was employed to examine the expressions of TGF-ß1, α-smooth muscle actin (α-SMA) and E-cadherin mRNA. RESULTS: HE and Masson staining showed that the renal interstitial of the rats in the control group had no significant fibrotic lesion; in the model group, there were obvious interstitial fibrosis; for the QCF group, there were epithelial cell necrosis, infiltration of lymphocytes and mononuclear cells, aggravated interstitial fibrosis in varied degrees, but the pathological changes were less in the QCF group than in the model group. The immunohistochemistry and Western blotting results showed that the TGF-ß1 expression was increased significantly in the model group, while decreased significantly in the QCF group (P<0.05); RT-PCR showed that the mRNA expression of α-SMA and TGF-ß1 increased significantly in the model group, while both were significantly decreased in the QCF group compared with the model group (P<0.05). The mRNA expression of E-cadherin was decreased significantly in the model group, and it was significantly increased in the QCF group as compared with the model group (P<0.05). CONCLUSION: QCF may improve renal fibrosis by regulating the expressions of TGF-ß1, α-SMA and E-cadherin, and prevent the progress of kidney fibrosis.

[Effects of dachengqi decoction containing serum on the expressions of caveolin-1, eNOS, and NF-kappaB in lipopolysaccharide stimulated human bronchial epithelial cells].

OBJECTIVE: To observe the effects of dachengqi decoction (DD) containing serum on the expressions of caveolin-1 (CAV-1), endothelial nitric oxide synthase (eNOS), and nuclear transcription factor-kappa B (NF-kappaB) in lipopolysaccharide (LPS) stimulated human bronchial epithelial cells (HBECs). METHODS: The DD and the DD containing serum were prepared. The in vitro cultured HBECs were randomly divided into 7 groups, i.e., the normal serum control group, the LPS intervention group, the low dose DD serum containing group, the middle dose DD serum containing group, the high dose DD serum containing group, the Western medicine control group, the vehicle serum control group. The effects of DD containing serum at different doses on the mRNA and protein expressions of CAV-1, eNOS, and NF-kappaB were detected using methyl thiazolyl tetrazolium (MTT) colorimetry, Real-time PCR, immunocytochemical assay, and Western blot. RESULTS: The mRNA and protein expressions of CAV-1, eNOS, and NF-kappaB at the basic levels were detected in the HBECs of the normal serum control group. After stimulated by LPS, the mRNA and protein expressions of CAV-1, eNOS, and NF-kappaB increased more significantly in the LPS intervention group than in the normal serum control group (P < 0.01), while DD containing serums at different doses all could suppress the mRNA and protein expressions of CAV-1, eNOS, and NF-kappaB. CONCLUSION: DD containing serum could inhibit the expressions of CAV-1, eNOS, and NF-kappaB in LPS stimulated HBECs.

[Effect of salvianolic acid B on CD14 expression in rats with liver fibrosis].

OBJECTIVE: To observe the effect of salvianolic acid B (SAB), an extract from Radix Salviae miltiorrhizae, on expression of leucocyte differentiation antigen 14 (CD14) in the liver tissue of experimental rats with carbon tetrachloride (CCl4)-induced liver fibrosis. METHODS: Thirty SD rats were randomly divided into three groups, the model group, the treated group, and the control group. The pathological fibrosis changes in liver of rats were observed. Meantime, their liver function was detected by automatic biochemical analyzer. Serum content of endotoxin was assayed by matrix staining, and plasma content of tumor necrosis factor-alpha (TNF-alpha) was detected by radioimmunoassay. mRNA and protein expressions of CD14 in the liver tissue were measured using reverse transcriptional-polymerase chain reaction and immunohistochemistry respectively. RESULTS: All the laboratory parameters, including liver function, degree of liver fibrosis, serum endotoxin levels, plasma TNF-alpha contents, and CD14 mRNA and protein expressions in the model group were higher than those in the control group (all P<0.01). All the aforesaid indices were lowered more in the treated group than in the model group (all P<0.01). CONCLUSIONS: SAB could antagonize the CCl4, induced liver fibrosis in rats. Its mechanism of action was possibly correlated with its effects on down-regulating hepatic CD14 expression and blocking the endotoxin signal transduction pathway.

Effect of Dachengqi decoction on NF-kappaB p65 expression in lung of rats with partial intestinal obstruction and the underlying mechanism.

To investigate the effect of Dachengqi decoction on NF-kappaB p65 expression in lung of rats with partial intestinal obstruction and the underlying mechanism, 30 SD rats were randomly divided into three groups: sham-operation group, model group and Dachengqi decoction treatment group (Dachengqi group), with 10 animals in each group. The models were made by partially ligating their large intestines outside the body. The pathological changes were analyzed by HE staining. The expression of NF-kappaB p65 in rats lung were measured by using real-time polymerase chain reaction and immunohistochemistry respectively. Moreover, the expression of caveolin-1 in rats lung was also measured to. Increased edema, interstitial thickening, hemorrhage, and infiltration of inflammatory cells were found in the model group. In contrast, this change was significantly reduced in Dachengqi group as compared with model group. In addition, the up-regulated caveolin-1 and NF-kappaB p65 were also suppressed by Dachengqi decoction in lung of rats with partial intestinal obstruction. We are led to concluded that the caveolin-1-NF-kappaB pathway plays an important role in the development of lung injury of rats with partial intestinal obstruction and Dachengqi decoction could down-regulate the expression of caveolin-1 and NF-kappaB p65 in lung of rats with partial intestinal obstruction.

[Experimental study on acting mechanism of vicera purging method in purging fu-organs and benefiting fei].

OBJECTIVE: To explore the acting mechanism of viscera purging method (VP) in purging Fu-organs and benefiting Fei from integral, cellular and molecular levels. METHODS: Forty SD rats were equally divided into four groups randomly: the normal group, the model group, the unhitch group and the VP group. Except those in the normal group were untreated, rats were established to intestinal obstruction model by incomplete ligation of the rectum in vitro. The ligation was relieved 48 h after operation in the unhitch group and the VP group, and the animals were fed continuously on routine. Meanwhile, Dachengqi Decoction (DD) 2 ml was given twice a day to the VP group for 2 days. Finally, the serum interleukin 8 (IL-8) and mRNA expression of tumor necrosis factor-alpha (TNF-alpha) in the lung tissue were detected by radioimmunoassay and RT-PCR respectively. Besides, the number of pulmonary alveolar macrophages (PAM) in the bronchial alveolus lavage fluid (BALF) was counted and their death rate calculated. RESULTS: Compared with the normal control, the serum IL-8 content in lung tissue in the model rats were remarkably higher (P < 0.01); however, the VP group showed the lowest level of IL-8 content and the highest was shown in the model group. Number of PAM in BALF was higher and its death rate was lower in the VP group than that in the unhitch groups (both P< 0.05). The expression of TNF-alpha mRNA was sinificantly higher as compared with that in the normal group, and lowered after administration of DD. CONCLUSION: Viscera purging method could protect the injured lung tissue to some extent.

Clinical study on therapy of clearing hallow viscera in treating critical patients with gastro-enteric function disorder.

OBJECTIVE: To explore the clinical effect of therapy of clearing hallow viscera in treating critical patients with gastro-enteric function disorder (GEFD). METHODS: Retrospective analysis was carried out on 96 critical patients. They were 48 patients in the treated group treated with Dachengqi Decoction and 48 patients in the control group treated with Western medicine for promoting gastric dynamic force. The recovery rate, recovery time of gastro-enteric function, incidence rate and fatality rate of multiple organ dysfunction syndrome (MODS), as well as the level of plasma endotoxin (ET) before and after treatment between the two groups were compared. RESULTS: Comparison between the two groups in gastro-enteric function recovery rate (81.3% vs 45.8%), functional disorder sustaining time in patients who got recovered (1.2 +/- 0.3 days vs 4.0 +/- 1.1 days), incidence rate (29.17% vs 52.08%) and fatality rate (28.57% vs 56.00%) of MODS all showed significant difference (P < 0.05 or P < 0.01). The plasma level of ET after treatment in the treated group was significantly lower than that in the control group (P < 0.05). CONCLUSION: Therapy of clearing hallow viscera has a good effect in treating critical patients with gastro-enteric function disorder, and could reduce the incidence and fatality of MODS.

[The protective effect of Rhadiola Astragalus Codonopsis compound on myocardium in early stage of severe burn at plateau in rats].

OBJECTIVE: To investigate the severity of early myocardial injury in rats with 30% full thickness burn at plateau and the protective effects of Rhadiola Astragalus Codonopsis Compound (RACC) on the rat myocardial injury. METHODS: One hundred and four Wistar rats with 30% full thickness burn were randomly divided into RACC application (R, n = 48) and scalding group 1 (S, n = 48), and another 8 healthy Wistar rats as control group 2 (C, n = 8). Four ml of RACC was garaged into the rat stomach in R and 4 ml isotonic saline in S groups respectively, but no treatment in C group. Blood samples from the aorta were harvested in 3, 6, 12, 24, 48 and 72 postburn hours (PBH) for blood gas analysis and for the determination of the changes in myocardial enzymes. Rat heart was harvested for pathomorphological examination. RESULTS: The rat myocardial tissue injury in R and S groups was obvious at 3 PBH and ameliorated gradually thereafter, up to the degree in C group at 72 PBH. The serum levels of myocardial enzymes in R and S groups were significantly higher than those in C group (P < 0.01). Whereas the enzymes in R group were much lower than those in S group (P < 0.01). It was indicated by blood gas analysis that the pH in R and S groups was lower than that in C group (P < 0.05), while that in R group at 12 - 24 PBH was higher than that in S group (P < 0.05). In addition, the base excess in R and S groups was lower than that in C group (P < 0.01), while that in R group at 6 PBH was higher than that in S group (P < 0.05 approximately 0.01). The PaCO2 in R and S groups was evidently lower than that in C group (P < 0.05 approximately 0.01), while that in R group at 48 PBH was no different to that in C group (35.70 +/- 4.23 mmHg vs 37.50 +/- 6.53 mmHg, P > 0.05). The PaO2 in R and S groups at 3 approximately 24 PBH was higher than that in C group and decreased gradually (P > 0.05). There was no difference in SaO2 among 3 groups (P > 0.05). CONCLUSION: RACC exhibited beneficial to the protection of rat heart from myocardial injury at plateau induced by severe burn.

Experimental study on the mechanism of protective effect of free Fu on gut-derived endotoxin-mediated lung damage.

The effect of tumor necrosis factor-alpha (TNF-alpha) on endotoxin (ET)-mediated lung damage caused by incomplete ligation of large intestine and the influence of free Fu on the expression of TNF-alpha mRNA were explored. Forty SD rats were randomly divided into 4 groups: normal control group, model group, ligation group and treatment group (n =10 in each group). The models were made by the method of partly ligating the rectum outside the body. The plasma level of lipopolysaccaride was measured by dynamic nephelo metric method and the serum level of TNF-alpha was detected by the method of radioactive immunity. The expression of TNF-alpha mRNA in lung tissue was detected by RT-PCR method. The results were compared among the 4 groups. The results showed the plasma levels of ET and serum TNF-alpha in the model group and the expression of TNF-alpha mRNA in the lung tissues were remarkably higher than those in the normal control group (P<0.01). After the treatment of free Fu, all of the above indexes in the treatment group were all decreased as compared with model group (all P<0.01), and the damage to lung was alleviated. It was concluded that TNF-alpha might play a very important role in the ET-mediated lung damage caused by incomplete ligation of large intestine, free Fu could protect the lung from damage.