The Role of Bioactives in Inflammation.

As a physiological defense mechanism, inflammation is a complex response to harmful stimuli [...].

Wild Bitter Melon Extract Abrogates Hypoxia-Induced Cell Death via the Regulation of Ferroptosis, ER Stress, and Apoptosis in Microglial BV2 Cells.

Microglial cells are well-known phagocytic cells that are resistant to the central nervous system (CNS) and play an important role in the maintenance of CNS homeostasis. Activated microglial cells induce neuroinflammation under hypoxia and typically cause neuronal damage in CNS diseases. In this study, we propose that wild bitter melon extract (WBM) has a protective effect on hypoxia-induced cell death via regulation of ferroptosis, ER stress, and apoptosis. The results demonstrated that hypoxia caused microglial BV-2 the accumulation of lipid ROS, ferroptosis, ER stress, and apoptosis. In this study, we investigated the pharmacological effects of WBM on BV-2 cells following hypoxia-induced cell death. The results indicated that WBM reversed hypoxia-downregulated antiferroptotic molecules Gpx4 and SLC7A11, as well as upregulated the ER stress markers CHOP and Bip. Moreover, WBM alleviated hypoxia-induced apoptosis via the regulation of cleaved-caspase 3, Bax, and Bcl-2. Our results suggest that WBM may be a good candidate for preventing CNS disorders in the future.

A case of methicillin resistant Staphylococcus aureus necrotizing pneumonia with pulmonary cryptococcosis.

A 37-year-old healthy man was transferred to the emergency department of this hospital because of fever and hemoptysis. A radiograph of the chest revealed a cavitary lesion in the right upper lobe. Computed tomography of the chest showed necrotizing cavitary pneumonia. Urgent throacoscopic lobectomy was performed. Sputum and intraoperative pleural pus grew methicillin resistant Staphylococcus aureus (MRSA). The pathological examination reportedly revealed cryptococcal infection. He had a full recovery after intravenous linezolid treatment.

Chrysophanol Prevents Lipopolysaccharide-Induced Hepatic Stellate Cell Activation by Upregulating Apoptosis, Oxidative Stress, and the Unfolded Protein Response.

Hepatic stellate cell (HSC) activation is a vital driver of liver fibrosis. Recent research efforts have emphasized the clearance of activated HSCs by apoptosis, senescence, or reversion to the quiescent state. LPS induces human HSC activation directly and contributes to liver disease progression. Chrysophanol is an anthraquinone with hepatoprotective and anti-inflammatory effects. This study aimed to investigate the pharmacological effects and mechanisms of chrysophanol in an LPS-induced activated rat HSC cell line (HSC-T6). The fibrosis phenotype was identified from the expression of α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF), and integrin ß1 by western blot analysis. We examined DNA fragmentation by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. We detected the apoptotic markers p53 and cleaved caspase-3 by western blot analysis. Intracellular ROS were labeled with 2',7'-dichlorofluorescein diacetate (DCF-DA) and the levels were measured by flow cytometry. Finally, we evaluated the ER stress markers binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP) by Western blot analysis. Our results showed that chrysophanol decreased HSC-T6 cell viability in LPS-induced activated HSCs. Chrysophanol increased the expression of α-SMA, CTGF, integrin ßI, p53, cleaved caspase-3, and DNA fragmentation. Chrysophanol also elevated ROS levels and increased the expression of BiP and CHOP. Pretreatment with chrysophanol prevented LPS-induced HSC-T6 cell activation by upregulating apoptosis, ROS accumulation, unfolded protein response (UPR) activation, and the UPR proapoptotic effect.

Apoptotic effects of hsian-tsao (Mesona procumbens Hemsley) on hepatic stellate cells mediated by reactive oxygen species and ERK, JNK, and caspase-3 pathways.

The activation of hepatic stellate cells (HSCs) is an important step in the progress of liver fibrosis. Fibrosis can be impeded by HSC reversion to a quiescent state or HSC clearance through apoptosis. To investigate the apoptotic effects of hsian-tsao (Mesona procumbens Hemsl) on human HSCs, the expression levels of cleaved caspase-3, p38, and c-Jun N-terminal kinase (JNK) were assessed using Western blotting, and the caspase-3 activity was measured using caspase-3/CPP32 colorimetric assay kit. Hsian-tsao extract (HTE) increased the activity of caspase-3 and the level of activated caspase-3, indicating the activation of apoptosis. The intracellular reactive oxygen species (ROS) level increased in a dose-dependent manner. This increase was prevented by an antioxidant, suggesting that HTE induces ROS accumulation. In addition, we found that HTE induced the phosphorylation of the mitogen-activated protein kinases JNK and p38. These collective data indicate that HTE induces apoptosis via ROS production through the p38, JNK, and caspase-3-dependent pathways. HTE may decrease HSC activation in liver fibrosis and may have a therapeutic potential.

Rapid creation of a temporary isolation ward for patients with severe acute respiratory syndrome in Taiwan.

OBJECTIVES: To rapidly establish a temporary isolation ward to handle an unexpected sudden outbreak of severe acute respiratory syndrome (SARS) and to evaluate the implementation of exposure control measures by healthcare workers (HCWs) for SARS patients. DESIGN: Rapid creation of 60 relatively negative pressure isolation rooms for 196 suspected SARS patients transferred from 19 hospitals and daily temperature recordings of 180 volunteer HCWs from 6 medical centers. SETTING: A military hospital. RESULTS: Of the 196 patients, 34 (17.3%) met the World Health Organization criteria for probable SARS with positive results of serologic testing for SARS-associated coronavirus (SARS-CoV), reverse transcriptase polymerase chain reaction (RT-PCR) from nasopharyngeal or throat swabs for SARS-CoV, or both. Seventy-four patients had suspected SARS based on unprotected exposure to SARS patients; three of them had positive results on RT-PCR but negative serologic results. The remaining 88 patients did not meet the criteria for a probable or suspected SARS diagnosis. Of the 34 patients with probable SARS, 13 were transferred to medical centers to receive mechanical ventilation due to rapid deterioration of chest x-ray results, and three patients died of SARS despite intensive therapy in medical centers. During the study period, one nurse developed probable SARS due to violation of infection control measures, but there was no evidence of cross-transmission to other HCWs. CONCLUSIONS: Despite the use of full personal protection equipment, the facility failed to totally prevent exposures of HCWs to SARS but minimized the risk of nosocomial transmission. Better training and improvements in infection control infrastructure may limit the impact of SARS.