RESUMO
SUMMARY: The Bactrian camel, which is native to China and Mongolia, is large in size and is an even-toed ungulate species. The double humps on the Bactrian camel back differentiate it from the dromedary camel, which has a single hump. This species has adapted to unsuitable conditions (lack of food and water) in the Gobi Desert and is advanced in unique anatomical and physiological characteristics during a prolonged evolution period. Several studies have been conducted on the anatomical features of the Bactrian camel, but none have given attention to the alveolar capillaries of the Bactrian camel lung. Therefore, the current study aims to explore the architecture of the alveolar capillary in the Bactrian camel lung and further explain the mechanism of blood flow in its lung. The current study extracted and examined the architecture of the alveolar capillary in the lung of the Bactrian camel (Camelus bactrianus) and further explained the mechanism of blood flow by performing lung casting and replica scanning electron microscopy methods. The reports showed that the resources of the alveolar-capillary originated from the capillaries of the subpleural space or interlobular septulum, sometimes originating from the precapillary arterioles or directly from the terminal arterioles. The alveolar capillaries anastomosed and formed a single layer of dense, basket-like network surrounding the alveolus. The mash diameter of the alveolar-capillary network was larger than that of the capillary, and the appearance of the mash was oval and elliptical. Many of the collapsed alveolar-capillary networks were found in the alveolar microvascular architecture in the lung of the Bactrian camel. The study found that, due to many collapsed alveoli in the Bactrian camel lung, the disproportional pressure between the pulmonary alveoli induced less imbalance of blood flow in the alveolar capillary, which affected the gas exchange efficiency. Therefore, the function of the anastomosing capillary branch was likely to regulate the blood flow between the alveolar-capillary network.
RESUMEN: El camello bactriano, es originario de China y Mongolia, es de gran tamaño y es una especie de ungulado de dedos pares. Las dobles jorobas del lomo del camello bactriano lo diferencian del dromedario, que tiene una sola joroba. Esta especie se ha adaptado a condiciones inadecuadas (falta de alimento y agua) en el desierto de Gobi y ha avanzado en características anatómicas y fisiológicas únicas durante un período de evolución prolongado. Se han realizado varios estudios sobre las características anatómicas del camello bactriano, pero ninguno ha prestado atención a los capilares alveolares del pulmón de este animal. Por lo tanto, el presente estudio tuvo como objetivo principal explorar la arquitectura del capilar alveolar en el pulmón del camello bactriano y explicar el mecanismo del flujo sanguíneo. A partir de nuestro trabajo se examinó la arquitectura del capilar alveolar en el pulmón del camello bactriano (Camelus bactrianus) mediante la realización de métodos de microscopía electrónica de barrido y escaneo pulmonar. Los informes mostraron que los recursos del alvéolo-capilar se originaban en los capilares del espacio subpleural o del tabique interlobulillar y a veces se originaban en las arteriolas precapilares o directamente en las arteriolas terminales. Los capilares alveolares se anastomosaban y formaban una densa red de capa única en forma de cesta que rodeaba el alvéolo. El diámetro del macerado de la red alveolar-capilar era mayor que el del capilar y el aspecto del macerado era ovalado y elíptico. Muchas de las redes alvéolo-capilares colapsadas se encontraron en la arquitectura microvascular alveolar en el pulmón del camello bactriano. El estudio encontró que, muchos alvéolos colapsados en el pulmón del camello bactriano, la presión desproporcionada entre los alvéolos pulmonares inducía un menor desequilibrio del flujo sanguíneo en el capilar alveolar, lo que afectaba la eficiencia del intercambio de gases. Por lo tanto, la función de la rama capilar anastomosante probablemente regularía el flujo sanguíneo entre la red alveolar-capilar.
Assuntos
Animais , Alvéolos Pulmonares/irrigação sanguínea , Alvéolos Pulmonares/ultraestrutura , Capilares/anatomia & histologia , Capilares/ultraestrutura , Camelus/anatomia & histologia , Pulmão/irrigação sanguínea , Pulmão/ultraestrutura , Microscopia Eletrônica de VarreduraRESUMO
INTRODUCTION AND OBJECTIVES: Necroptosis and endoplasmic reticulum (ER) stress has been implicated in acute and chronic liver injury. Activated eukaryotic initiation factor 2 alpha (eIF2α) attenuates protein synthesis and relieves the load of protein folding in the ER. In this study, we aimed to analyze the impact of eIF2α phosphorylation on hepatocyte necroptosis in acute liver injury. MATERIALS AND METHODS: Male BALB/c mice were injected with tunicamycin or d-galactosamine, and LO2 cells were incubated with tunicamycin to induce acute liver injury. 4-Phenylbutyric acid (PBA) and salubrinal were used to inhibit ER stress and eIF2α dephosphorylation, respectively. We analyzed the eIF2α phosphorylation, ER stress, and hepatocyte necroptosis in mice and cells model. RESULTS: Tunicamycin or d-galactosamine significantly induced ER stress and necroptosis, as well as eIF2α phosphorylation, in mice and LO2 cells (p<0.05). ER stress aggravated tunicamycin-induced hepatocyte necroptosis in mice and LO2 cells (p<0.05). Elevated eIF2α phosphorylation significantly mitigated hepatocyte ER stress (p<0.05) and hepatocyte necroptosis in mice (34.37±3.39% vs 22.53±2.18%; p<0.05) and LO2 cells (1±0.11 vs 0.33±0.05; p<0.05). Interestingly, tumor necrosis factor receptor (TNFR) 1 protein levels were not completely synchronized with necroptosis. TNFR1 expression was reduced in d-galactosamine-treated mice (p<0.05) and cells incubated with tunicamycin for 12 and 24h (p<0.05). ER stress partially restored TNFR1 expression and increased necroptosis in tunicamycin-incubated cells (p<0.05). CONCLUSIONS: These results imply that ER stress can mediate hepatocyte necroptosis independent of TNFR1 signaling and elevated eIF2α phosphorylation can mitigate ER stress during acute liver injury.