Using new indices to predict metabolism dysfunction-associated fatty liver disease (MAFLD): analysis of the national health and nutrition examination survey database.

Background: Metabolism dysfunction-associated fatty liver disease (MAFLD), is the most common chronic liver disease. Few MAFLD predictions are simple and accurate. We examined the predictive performance of the albumin-to-glutamyl transpeptidase ratio (AGTR), plasma atherogenicity index (AIP), and serum uric acid to high-density lipoprotein cholesterol ratio (UHR) for MAFLD to design practical, inexpensive, and reliable models.

Resolvin D1 Induces mTOR-independent and ATG5-dependent Autophagy in BV-2 Microglial Cells.

Objective: The activation state of microglia is known to occupy a central position in the pathophysiological process of cerebral inflammation. Autophagy is a catabolic process responsible for maintaining cellular homeostasis. In recent years, autophagy has been demonstrated to play an important role in neuroinflammation.

Aldehyde Dehydrogenase 2 Preserves Mitochondrial Function in the Ischemic Heart: A Redox-dependent Mechanism for AMPK Activation by Thioredoxin-1.

Aldehyde dehydrogenase 2 (ALDH2) protects the ischemic heart by activating adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling. However, the molecular mechanisms linking ALDH2 and AMPK signaling are not fully understood. This study aimed to explore the potential mechanisms linking ALDH2 and AMPK in myocardial ischemic injury.

Mechanosensitive ion channel Piezo1 mediates mechanical ventilation-exacerbated ARDS-associated pulmonary fibrosis.

Introduction: Pulmonary fibrosis is a major cause of the poor prognosis of acute respiratory distress syndrome (ARDS). While mechanical ventilation (MV) is an indispensable life-saving intervention for ARDS, it may cause the remodeling process in lung epithelial cells to become disorganized and exacerbate ARDS-associated pulmonary fibrosis. Piezo1 is a mechanosensitive ion channel that is known to play a role in regulating diverse physiological processes, but whether Piezo1 is necessary for MV-exacerbated ARDS-associated pulmonary fibrosis remains unknown.

Immunothrombosis in Acute Respiratory Dysfunction of COVID-19.

COVID-19 is an acute, complex disorder that was caused by a new β-coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Based on current reports, it was surprising that the characteristics of many patients with COVID-19, who fulfil the Berlin criteria for acute respiratory distress syndrome (ARDS), are not always like those of patients with typical ARDS and can change over time. While the mechanisms of COVID-19-related respiratory dysfunction in COVID-19 have not yet been fully elucidated, pulmonary microvascular thrombosis is speculated to be involved.

Glucocorticoid-Induced Leucine Zipper: A Promising Marker for Monitoring and Treating Sepsis.

Sepsis is a clinical syndrome that resulting from a dysregulated inflammatory response to infection that leads to organ dysfunction. The dysregulated inflammatory response transitions from a hyper-inflammatory phase to a hypo-inflammatory or immunosuppressive phase. Currently, no phase-specific molecular-based therapies are available for monitoring the complex immune response and treating sepsis due to individual variations in the timing and overlap of the dysregulated immune response in most patients.

Structure, kinetic properties and biological function of mechanosensitive Piezo channels.

Mechanotransduction couples mechanical stimulation with ion flux, which is critical for normal biological processes involved in neuronal cell development, pain sensation, and red blood cell volume regulation. Although they are key mechanotransducers, mechanosensitive ion channels in mammals have remained difficult to identify. In 2010, Coste and colleagues revealed a novel family of mechanically activated cation channels in eukaryotes, consisting of Piezo1 and Piezo2 channels.

Curcumin Promotes Apoptosis of Activated Hepatic Stellate Cells by Inhibiting Protein Expression of the MyD88 Pathway.

Activation and proliferation of hepatic stellate cells (HSC) play an important role in the progress of liver fibrosis. HSC activation occurs in response to inflammatory cytokines, cellular interactions with immune cells, and morphogenetic signals. The literature hints to a role of the adaptor protein MyD88 in fibrosis.

Curcumin, the main active constituent of turmeric (Curcuma longa L.), induces apoptosis in hepatic stellate cells by modulating the abundance of apoptosis-related growth factors.

In order to elucidate the mechanism of action of curcumin against hepatic fibrosis, cultured rat hepatic stellate cells (HSC) (HSC-T6) were incubated with curcumin for 24 h, after which apoptosis was measured by flow-cytometry. The protein levels of the pro-apoptotic factors Fas and p53b as well as of the anti-apoptotic factor Bcl-2 were monitored by immunocytochemical ABC staining after incubation with curcumin for 24 h. In the case of 20 μM curcumin, not only was the respective apoptosis index increased, but also the abundance of the pro-apoptotic factors Fas and p53 were amplified, whereas that of the anti-apoptotic factor Bcl-2 decreased.

Induction of autophagy and apoptosis by miR-148a through the sonic hedgehog signaling pathway in hepatic stellate cells.

Autophagy is an evolutionarily conserved biological process that is activated in response to stress. Increasing evidence indicate that dysregulated miRNAs significantly contribute to autophagy and are thus implicated in various pathological conditions, including hepatic fibrosis. MiR-148a, a member of the miR-148/152 family, has been found to be downregulated in hepatic fibrosis and human hepatocellular carcinoma.

Transforming growth factor‑β1 reduces apoptosis via autophagy activation in hepatic stellate cells.

Autophagy is a metabolic process that is important in fibrogenesis, in which cellular components are degraded by lysosomal machinery. Transforming growth factor β1 (TGF‑β1) is a potent fibrogenic cytokine involved in liver fibrosis; however, it remains elusive whether autophagy is regulated by TGF‑β1 in this process. In the present study, the function of TGF‑β1‑mediated autophagy in the proliferation and apoptosis of hepatic stellate cells (HSCs) was investigated.

[Effects of nerve growth factor on proliferation of hepatic stellate cells].

Objective: To determine the effects of nerve growth factor (NGF) on proliferation of hepatic stellate cells (HSCs) and investigate the related molecular mechanism.

Methods: After incubating cultured HSCs for 24 h with different concentrations of NGF (100, 200 or 400 ng/mL), the cell proliferation was observed by XTT colorimetric assay and cell cycle was detected by flow cytometry. Morphological changes in response to a 24 h exposure to 100 ng/mL NGF were observed by transmission electron microscopy.

The inhibitory effect of 20(S)-protopanaxatriol (ppt) towards UGT1A1 and UGT2B7.

Ginseng, a commonly used natural product, has been frequently reported to induce herb-drug interaction with many clinical drugs. The intestinal bacterial metabolites of ginsenosides have been widely regarded as the substance basis for ginseng-drug interactions. To date, little is known about the inhibitory effect of intestinal bacterial metabolites of ginsenosides towards UDP-glucuronosyltransferases (UGTs).

Identification and determination of the major constituents in traditional Chinese medicine Longdan Xiegan Pill by HPLC-DAD-ESI-MS.

A novel and sensitive HPLC-UV method has been developed for the simultaneous determination of twelve major compounds in Longdan Xiegan Pill. The chemical profile of the twelve compounds, including geniposidic acid (1), geniposide(2), gentiopicroside(3), liquiritin(4), crocin(5), baicalin(6), wogonoside(7), baicalein(8), glycyrrhizic acid (9), wogonin (10), oroxylin A (11) and aristolochic acid A (12), was acquired using high-performance liquid chromatography-diode array detector coupled with an electrospray tandem mass spectrometer (HPLC-DAD-ESI-MS). The analysis was performed on a Dikma Platisil ODS C column (250 mm × 4.

[Preliminary study on mechanism of therapeutic effect of Huganjiexian decoction on hepatic fibrosis].

Objective: To observe the effects of Huganjiexian decoction on rat hepatic fibrosis and the creation of cytokines.

Methods: Rat hepatic fibrosis was induced by intraperitoneally injection of carbon tetrachloride. At the same time, these rats were treated with different dosages of Huganjiexian decoction.

Curcumin prevents liver fibrosis by inducing apoptosis and suppressing activation of hepatic stellate cells.

This study was designed to investigate the prophylactic effects and the mechanisms of curcumin on liver fibrosis in rats. Liver fibrosis was induced in 72 Sprague Dawley rats by intraperitoneal injection of carbon tetrachloride. Rats were divided into control, liver fibrosis, high, medium, and low dose curcumin (200, 100, and 50 mg kg(-1), respectively), and colchicine (0.

[The role and mechanisms of cyclooxygenase-2 inhibitors on the proliferation of hepatic stellate cell].

Objectives: To observe the effects of NS-398 on proliferation of hepatic stellate cells (HSCs) in vitro, and to investigate the possible molecule mechanism.

Methods: HSCs were incubated with different concentrations of NS-398. The effects of NS-398 on cell proliferation was detected by MTT colormetric assay.

[The study of therapeutic effects of curcumin on hepatic fibrosis and variation of correlated cytokine].

Objective: To investigate therapeutic effects of curcumin on hepatic fibrosis and the variation of correlated cytokine.

Methods: Rat models of hepatic fibrosis were made by carbon tetrachloride. Curcumin of 10, 20, 40 mg per 100 gram weight of rat were given to these rats of curcumin group respectively from ninth week.

[Prophylactic effect of curcumin on hepatic fibrosis and its relationship with activated hepatic stellate cells].

Objective: To observe the prophylactic effect of curcumin on hepatic fibrosis and the number, location, apoptosis of activated hepatic stellate cells (HSCs) in the livers and to discuss the relationship between the prophylactic effects and activated HSC.

Methods: A rat model of hepatic fibrosis was established by intraperitoneal injection of carbon tetrachloride. Curcumin doses of 5 mg, 10 mg, 20 mg per 100 gram per 100g of body weight were given to three groups of the model rats.