Curcumin regulates pulmonary extracellular matrix remodeling and mitochondrial function to attenuate pulmonary fibrosis by regulating the miR-29a-3p/DNMT3A axis.

Epigenetic regulation and mitochondrial dysfunction are essential to the progression of idiopathic pulmonary fibrosis (IPF). Curcumin (CCM) in inhibits the progression of pulmonary fibrosis by regulating the expression of specific miRNAs and pulmonary fibroblast mitochondrial function; however, the underlying mechanism is unclear. C57BL/6 mice were intratracheally injected with bleomycin (5 mg/kg) and treated with CCM (25 mg/kg body weight/3 times per week, intraperitoneal injection) for 28 days. Verhoeff-Van Gieson, Picro sirius red, and Masson's trichrome staining were used to examine the expression and distribution of collagen and elastic fibers in the lung tissue. Pulmonary fibrosis was determined using micro-computed tomography and transmission electron microscopy. Human pulmonary fibroblasts were transfected with miR-29a-3p, and RT-qPCR, immunostaining, and western blotting were performed to determine the expression of DNMT3A and extracellular matrix collagen-1 (COL1A1) and fibronectin-1 (FN1) levels. The expression of mitochondrial electron transport chain complex (MRC) and mitochondrial function were detected using western blotting and Seahorse XFp Technology. CCM in increased the expression of miR-29a-3p in the lung tissue and inhibited the DNMT3A to reduce the COL1A1 and FN1 levels leading to pulmonary extracellular matrix remodeling. In addition, CCM inhibited pulmonary fibroblasts MRC and mitochondrial function via the miR-29a-3p/DNMT3A pathway. CCM attenuates pulmonary fibrosis via the miR-29a-3p/DNMT3A axis to regulate extracellular matrix remodeling and mitochondrial function and may provide a new therapeutic intervention for preventing pulmonary fibrosis.

Extracorporeal membrane oxygenation to support prolonged conventional cardiopulmonary resuscitation in adults with cardiac arrest from acute myocardial infarction at a very low-volume centre.

We aimed to analyse the outcomes of the deployment of extracorporeal membrane oxygenation assisted cardiopulmonary resuscitation (E-CPR) 11 times for acute myocardial infarction (AMI) in 10 adult patients at a very low-volume (VLV) centre, where perfusionists or surgeons are not always available. We conducted a three-year retrospective chart review. E-CPR was performed 13 times in 12 adult patients who had cardiac arrest events and who underwent conventional CPR for longer than 10 min. We excluded other aetiologies that led to E-CPR. All 11 selected episodes of E-CPR were diagnosed as AMI. Seven patients (63.6%) were successfully weaned off extracorporeal membrane oxygenation (ECMO). Four patients survived to discharge without neurological deficits or other postE-CPR complications (36.3%). Seven patients died after E-CPR, and with one patient, there was no return of spontaneous beating during E-CPR (0.9%). Three patients died of unstable haemodynamics despite revascularisation of the coronary circulation. Three patients were successfully weaned off ECMO; however, they died subsequently of multiple organ dysfunction, unstable haemodynamic changes and septic shock from nosocomial infections, respectively. The outcome of E-CPR in adults with AMI was compared with previous studies at high-volume centres. Mortality or morbidity rates are not higher at a VLV centre.