The Short and Long Term Consequences of Delayed Cord Clamping on Late Pre-Term Infants.

Objective: To explore the effect of delayed cord clamping on preterm infants. Methods: A retrospective analysis was conducted using the clinical data of 163 preterm infants with a gestational age of 34-36 weeks + 6 who were admitted to the neonatology department within 2 hours after birth. The blood routine examination indices within 2 hours and at 3-5 days after birth, the biochemical indices and arterial blood gas (ABG) indices within 2 hours after birth, and the hemoglobin level 5-6 months after birth were compared between the early cord clamping (ECC) group and the delayed cord clamping (DCC) group. Results: Compared with the ECC group, the DCC group had significantly higher venous blood levels of red blood cells, hemoglobin, and hematocrit within 2 hours and at 3-5 days after birth. The ABG bicarbonate (HCO3) level within 2 hours after birth was obviously higher in the DCC group than in the ECC group, and the ABG absolute base excess(BE) and lactate levels were lower in the DCC group than in the ECC group (P < 0.05). There was no significant difference between the two groups in the incidence of hypothermia, hypoglycemia, respiratory distress, septicemia, feeding intolerance, polycythemia, and hyperbilirubinemia requiring phototherapy during hospitalization (P > 0.05). Compared with the ECC group, the DCC group had a significantly higher venous blood hemoglobin level 5-6 months after birth. The incidence of anemia in the DCC group was significantly lower than in the ECC group (P < 0.05). Conclusion: Delayed cord clamping can significantly increase the hemoglobin levels of preterm infants at birth and at 5-6 months after birth and can improve the oxygen circulation supply to the organs of such infants. Therefore, delayed cord clamping can improve the prognosis of preterm infants.

Epigallocatechin-3-gallate attenuates acute pancreatitis induced lung injury by targeting mitochondrial reactive oxygen species triggered NLRP3 inflammasome activation.

Green tea has been considered as a health-promoting beverage and is widely consumed worldwide. Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol derived from green tea leaves with potent antioxidative and chemopreventive activities, has been reported to offer protection against inflammation-driven tissue damage. Here, we evaluated the protective effects of EGCG against lung injury during acute pancreatitis (AP) and further revealed the detailed mechanism. The results showed that EGCG significantly attenuated l-arginine-induced AP and the consequent pulmonary damage in mice. Moreover, EGCG substantially attenuated oxidative stress and concurrently suppressed NOD-like receptor protein 3 (NLRP3) inflammasome activation in the lung. In vitro, EGCG considerably reduced the production of mitochondrial reactive oxygen species (mtROS) and oxidized mitochondrial DNA (ox-mtDNA) in alveolar macrophages (AMs) challenged with AP-conditioned plasma. Meanwhile, the amount of ox-mtDNA bound to NLRP3 decreased significantly by the treatment with EGCG, resulting in impaired NLRP3 inflammasome activation. In addition, the antagonism of NLRP3 signaling by EGCG was affected in the presence of the mtROS stimulant rotenone or scavenger Mito-TEMPO. Altogether, EGCG possesses potent activity to attenuate lung injury during AP progression by inhibiting NLRP3 inflammasome activation. As for the mechanism, the EGCG-conferred restriction of NLRP3 inflammasome activation probably arises from the elimination of mtROS as well as its oxidative product ox-mtDNA, which consequently enables the protection against AP-associated lung injury.