Liang-Ge-San Decoction Ameliorates Acute Respiratory Distress Syndrome via Suppressing p38MAPK-NF-κ B Signaling Pathway.

Objective: To explore the potential effects and mechanisms of Liang-Ge-San (LGS) for the treatment of acute respiratory distress syndrome (ARDS) through network pharmacology analysis and to verify LGS activity through biological experiments.

Methods: The key ingredients of LGS and related targets were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. ARDS-related targets were selected from GeneCards and DisGeNET databases.

[Mechanism of Xuebijing Injection in treatment of sepsis-associated ARDS based on network pharmacology and in vitro experiment].

The aim of this study was to investigate the effect and molecular mechanism of Xuebijing Injection in the treatment of sepsis-associated acute respiratory distress syndrome(ARDS) based on network pharmacology and in vitro experiment. The active components of Xuebijing Injection were screened and the targets were predicted by the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP). The targets of sepsis-associated ARDS were searched against GeneCards, DisGeNet, OMIM, and TTD.

[Mechanism of modified Liangge San in treatment of acute respiratory distress syndrome based on network pharmacology and experimental validation].

A network pharmacology-based strategy combined with molecular docking and in vitro validation was employed to investigate potential targets and molecular mechanisms of modified Liangge San(MLGS) against acute respiratory distress syndrome(ARDS). Active ingredients and corresponding targets of MLGS were screened out on the Traditional Chinese Medicines Systems Pharmacology(TCMSP) database, and the disease targets of ARDS were obtained by integrating GeneCards and DisGeNET database. The two were intersected to obtain the potential targets of MLGS against ARDS.

Arctigenin attenuates paraquat-induced human lung epithelial A549 cell injury by suppressing ROS/p38 mitogen-activated protein kinases-mediated apoptosis.

Background: Paraquat (PQ)-induced acute lung injury (ALI) and pulmonary fibrosis are common diseases with high mortality but without effective antidotes in emergency medicine. Our previous study has proved that arctigenin suppressed pulmonary fibrosis induced by PQ. We wondered whether arctigenin could also have a protective effect on PQ-induced ALI.

Pravastatin attenuates sepsis-induced acute lung injury through decreasing pulmonary microvascular permeability via inhibition of Cav-1/eNOS pathway.

Background: Disruption of alveolar endothelial barrier caused by inflammation drives the progression of septic acute lung injury (ALI). Pravastatin, an inhibitor of HMG Co-A reductase, has potent anti-inflammatory effects. In the present study, we aim to explore the beneficial role of pravastatin in sepsis-induced ALI and its related mechanisms.

Pretreatment with intestinal trefoil factor alleviates stress-induced gastric mucosal damage Akt signaling.

Background: Stress-related gastric mucosal damage or ulcer remains an unsolved issue for critically ill patients. Stress ulcer prophylaxis has been part of routine intensive care, but uncertainty and controversy still exist. Co-secreted with mucins, intestinal trefoil factor (ITF) is reported to promote restitution and regeneration of intestinal mucosal epithelium, although the mechanism remains unknown.

[Effects of Rg_1 on LPS-induced apoptosis and autophagy of lung epithelial cells].

This paper aimed to study the protective effect of ginsenoside Rg_1 on endotoxin(LPS)-induced apoptosis of lung epithelial cells and its mechanism of action. Mouse lung epithelial cells(MLE-12) were first treated with LPS. The autophagy changes and apoptosis and the relationship with concentration and time of LPS were observed.

S100B protein in serum is elevated after global cerebral ischemic injury.

Background: S100B protein in patients with cardiac arrest, hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased. Ischemic brain injury may elevate the level of serum S100B protein and the severity of brain damage.

Methods: This article is a critical and descriptive review on S100B protein in serum after ischemic brain injury.

Effect of penehyclidine hydrochloride on patients with acute lung injury and its mechanisms.

Objective: To assess the effects of penehyclidine hydrochloride on patients with acute lung injury (ALI), to observe the expression of Toll-like receptor 4 (TLR4) on the peripheral monocytes of ALI patients and changes of inflammatory and anti-inflammatory cytokines and to investigate the mechanism of TLR4 in ALI.

Methods: Forty-five patients with ALI were randomly divided into penehyclidine hydrochloride treatment group (P group, n equal to 21) and conventional treatment group (control group, C group, n equal to 24). Patients in both groups received conventional treatment, including active treatment of the primary disease, respiratory support, nutritional support and fluid management therapy, while those in P group were given penehyclidine hydrochloride (1 mg, im, q.

[Role of trefoil peptides in modulation of gastric adaptation to stress].

Objective: To investigate the role of trefoil peptides in modulation of gastric adaptation to water restraint stress (WRS) in rats.

Methods: Wistar rats were exposed to single or repeated WRS for 4 hours every other day for up to 6 days, gastric mucosal blood flow (GMBF) was measured by LDF-3 flowmeter, the extent of gastric mucosal lesions was evaluated grossly and histologically, and expression of PS2 intestinal trefoil peptide (ITF), cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS) and transferase growth factor-alpha (TGF-alpha) were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.

Results: One application of WRS produced extensive gastric mucosal erosion.

Serial analysis of gene expression in mice with lipopolysaccharide-induced acute lung injury.

Objective: To monitor the systemic gene expression profile in a murine model of lipopolysaccharide-induced acute lung injury.

Methods: Acute lung injury was induced by intratracheal injection of lipopolysaccharide in 3 mice. Another 3 normal mice receiving same volume of normal saline were taken as the controls.

Cyclooxygenase 2, pS2, inducible nitric oxide synthase and transforming growth factor alpha in gastric adaptation to stress.

Aim: To determine the role of mucosal gene expression of cyclooxygenase 2 (COX-2), pS2 (belongs to trefoil peptides), inducible nitric oxide synthase (iNOS) and transforming growth factor alpha (TGFalpha) in gastric adaptation to water immersion and restraint stress (WRS) in rats.

Methods: Wistar rats were exposed to single or repeated WRS for 4 h every other day for up to 6 d. Gastric mucosal blood flow (GMBF) was measured by laser Doppler flowmeter-3.

Role of TFF in healing of stress-induced gastric lesions.

Aim: To determine the changes of pS2 and ITF of TFF expression in gastric mucosa and the effect on ulcer healing of pS2, ITF to Water-immersion and restraint stress (WRS) in rats.

Methods: Wistar rats were exposed to single or repeated WRS for 4 h every other day for up to 6 days.Gastric mucosal blood flow (GMBF) was measured by LDF-3 flowmeter and the extent of gastric mucosal lesions were evaluated grossly and histologically.

[Relation between nitric oxide synthase, psychology, gastric mucosal blood flow and gastric mucosal adaptive cytoprotection under stress in rats].

Objective: To explore the relation between nitric oxide synthase (NOS), psychology, gastric mucosal blood flow(GMBF) and gastric mucosal adaptive cytoprotection under stress in rats and its possible mechanism.

Methods: Animal model was constructed with impulsive stimulator of high voltage and stable currency, seventy-two male SD rats were randomly divided into three groups: control(C), regular(R) and irregular(I) group. NOS activity was measured by spectrophotometry and injure of gastric mucosa was measured by method of Nils Lambecht, GMBF was measured by LDF-3 flowmeter.