High-Throughput Screening of an FDA-Approved Compound Library Reveals a Novel GAS6 Receptor Agonist for Therapeutic Intervention in Septic Myocardial and microvascular Injury via Modulation of Danger-Associated Molecular Patterns.

PGAM5 and VDAC1 have both been reported to regulate mitophagy. However, the mechanisms by which they regulate sepsis-induced inflammatory microvascular injury remain unverified. In previous studies, we established the role of this regulatory axis in various phenotypic processes, including mitophagy, mitochondrial biogenesis, the mitochondrial unfolded protein response, and mitochondrial dynamics, while further confirming the interactive regulatory proteins within this axis.

Protective Effects of Necrostatin-1 in Acute Pancreatitis: Partial Involvement of Receptor Interacting Protein Kinase 1.

Acute pancreatitis (AP) is a severe and potentially fatal disease caused predominantly by alcohol excess and gallstones, which lacks a specific therapy. The role of Receptor-Interacting Protein Kinase 1 (RIPK1), a key component of programmed necrosis (Necroptosis), is unclear in AP. We assessed the effects of RIPK1 inhibitor Necrostatin-1 (Nec-1) and RIPK1 modification (RIPK1: kinase dead) in bile acid (TLCS-AP), alcoholic (FAEE-AP) and caerulein hyperstimulation (CER-AP) mouse models.

Knockout of the Mitochondrial Calcium Uniporter Strongly Suppresses Stimulus-Metabolism Coupling in Pancreatic Acinar Cells but Does Not Reduce Severity of Experimental Acute Pancreatitis.

Acute pancreatitis is a frequent disease that lacks specific drug treatment. Unravelling the molecular mechanisms of acute pancreatitis is essential for the development of new therapeutics. Several inducers of acute pancreatitis trigger sustained Ca increases in the cytosol and mitochondria of pancreatic acinar cells.

Corrigendum to "Cardioprotective Effects of Qishenyiqi Mediated by Angiotensin II Type 1 Receptor Blockade and Enhancing Angiotensin-Converting Enzyme 2".

[This corrects the article DOI: 10.1155/2012/978127.].

Oxidative stress alters mitochondrial bioenergetics and modifies pancreatic cell death independently of cyclophilin D, resulting in an apoptosis-to-necrosis shift.

Mitochondrial dysfunction lies at the core of acute pancreatitis (AP). Diverse AP stimuli induce Ca-dependent formation of the mitochondrial permeability transition pore (MPTP), a solute channel modulated by cyclophilin D (CypD), the formation of which causes ATP depletion and necrosis. Oxidative stress reportedly triggers MPTP formation and is elevated in clinical AP, but how reactive oxygen species influence cell death is unclear.

Metabolomic profiling reveals distinct patterns of tricarboxylic acid disorders in blood stasis syndrome associated with coronary heart disease.

Objective: To investigate the underlying metabolomic profifiling of coronary heart disease (CHD) with blood stasis syndrome (BSS).

Methods: CHD model was induced by a nameroid constrictor in Chinese miniature swine. Fifteen miniature swine were randomly divided into a model group (n=9) and a control group (n=6), respectively according to arandom number table.

Caffeine protects against experimental acute pancreatitis by inhibition of inositol 1,4,5-trisphosphate receptor-mediated Ca2+ release.

Objective: Caffeine reduces toxic Ca signals in pancreatic acinar cells via inhibition of inositol 1,4,5-trisphosphate receptor (IPR)-mediated signalling, but effects of other xanthines have not been evaluated, nor effects of xanthines on experimental acute pancreatitis (AP). We have determined effects of caffeine and its xanthine metabolites on pancreatic acinar IPR-mediated Ca signalling and experimental AP.

Design: Isolated pancreatic acinar cells were exposed to secretagogues, uncaged IP or toxins that induce AP and effects of xanthines, non-xanthine phosphodiesterase (PDE) inhibitors and cyclic adenosine monophosphate and cyclic guanosine monophosphate (cAMP/cGMP) determined.

Effects of Sini San used alone and in combination with fluoxetine on central and peripheral 5-HT levels in a rat model of depression.

Objective: To investigate the effects of Sini San and fluoxetine on the levels of central and peripheral 5-HT in a rat model of depression, and provide new insight into the treatment of depression with integrated Chinese-Western Medicine.

Methods: A rat model of depression was established by chronic mild stress (CMS). Model rats received either Sini San, fluoxetine, a combination of the two drugs, or no drug treatment.

Integrated proteomic and metabolomic analysis reveals the NADH-mediated TCA cycle and energy metabolism disorders based on a new model of chronic progressive heart failure.

Background: Despite major advances in the treatment of heart failure (HF), it remains the major cause of mortality and morbidity worldwide. Experimental models of HF typically utilize acute myocardial infarction. However, the majority of clinical HFs occur gradually by a chronic progressive mechanism.

Cardioprotective Effects of Qishenyiqi Mediated by Angiotensin II Type 1 Receptor Blockade and Enhancing Angiotensin-Converting Enzyme 2.

The aim of this paper was to investigate whether the effects of QSYQ on CHD are associated with the renin-angiotensin-aldosterone system (RAAS). The formula groups were lavaged with QSYQ, using fosinopril sodium as a control. The level of RAAS components in the myocardial tissue was measured, respectively.

The active ingredients of Jiang-Zhi-Ning: study of the Nelumbo nucifera alkaloids and their main bioactive metabolites.

The object of this study was to identify the major active ingredients of the Chinese Traditional Medicine Jiang-Zhi-Ning (JZN) based on the high performance liquid chromatography (HPLC) profiles of plasma samples obtained from beagle dogs at different times after intragastric administration of JZN, crude JZN extracts, different extracted fractions, different subfractions of the active fraction and different isolated ingredients. 2-Hydroxy-1-methoxyaporphin (2H1M), an alkaloid from Nelumbo nucifera, one of the herbs that make up JZN, was identified as the constituent showing the major pharmacodynamic effect. The major metabolites of 2H1M were analyzed and identified as N-demethyl-2-hydroxy-1-methoxyaporphine-2-O-glycuronic acid, 2-hydroxy-1-methoxy-aporphine-2-O-glycuronic acid and 2-hydroxy-1-methoxy-aporphine-2-O-sulphate.

[Effects of a compound Chinese herbal medicine Yixin Jiedu formula on haemodynamic in rats with heart failure of qi-deficiency and blood stasis syndrome].

Objective: To explore the effects of Yixin Jiedu Formula (YXJDF), a compound Chinese herbal medicine, on hemodynamic and B-type natriuretic (BNP) in a rat model of heart failure with qi deficiency and blood stasis syndrome. Moreover, its therapeutic effects in improving the symptoms were also studied.

Methods: The model of heart failure was established by ligation of left coronary artery in rats.

Drug target prediction based on the herbs components: the study on the multitargets pharmacological mechanism of qishenkeli acting on the coronary heart disease.

In this paper, we present a case study of Qishenkeli (QSKL) to research TCM's underlying molecular mechanism, based on drug target prediction and analyses of TCM chemical components and following experimental validation. First, after determining the compositive compounds of QSKL, we use drugCIPHER-CS to predict their potential drug targets. These potential targets are significantly enriched with known cardiovascular disease-related drug targets.