白细胞游走到损伤区吞噬细菌并通过释放毒素分子和生化物质破坏细菌。
They swarm to the injury to engulf and destroy bacteria with toxic molecules and biochemicals.
尿毒症毒素通过影响线粒体功能而导致细胞损伤。
In CRF, uremic toxins injured cell by influencing mitochondria.
比较了微囊藻毒素-LR (MC - LR)对两类细胞的DNA损伤差异。
To compare DNA damage induced by microcystin-LR (MC-LR) in two kinds of cell lines.
目的：研究表皮细胞生长因子雾化吸入对内毒素所致急性肺损伤的治疗作用。
Objective:To study the effects of inhalation of epidermal growth factor aerosol on endotoxin-induced acute lung injury.
结论罗红霉素能改善大鼠急性肺损伤时气体交换能力，调节肺部细胞因子，对内毒素诱导的急性肺损伤有保护作用。
CONCLUSION Roxithromycin has a protective effect on rat acute lung injury induced by LPS through regulating cytokines, improving gas exchange ability, and inhibiting lung permeability.
提高防疫功能，减少外界毒素对皮肤的损伤，延缓衰老。使皮肤干扁细胞短时间回复活力，显出饱满、亮泽、紧致、细腻的完美肌肤。
Strengthen immunity, protect skin from external toxin, fight ageing, boost vigor of dry and withered skin cells, and make skin smooth, lustrous, firm, tender and perfect.
目的探讨内毒素肺损伤时，肺泡巨噬细胞逐步由免疫防御型转变为效应型的分子机制。
Objective To study the molecular mechanism of the conversion of alveolar macrophages (AMs) from immune defensive cells to effective cells in mice with endotoxin induced lung injury.
目的探讨分泌型白细胞蛋白酶抑制剂（SLPI）对内毒素（LPS）致新生大鼠急性肺损伤（ALI）的抗感染作用。
Objective To investigate the anti-inflammatory effects of secretory leukocyte protease inhibitor(SLPI) on newborn rats with lipopolysaccharide(LPS)-induced acute lung injury(ALI).
在促炎症反应如内毒素、缺血再灌注损伤和免疫反应中，过量释放的细胞因子和前列腺素样物质可引起肝损伤。
During proinflammatory reactions such as endotoxemia, ischemia - reperfusion and immune reactions, excessive amounts of cytokines and prostanoids are released resulting in liver injury.
霉菌毒素影响细胞的生长，通过增加细胞内活性氧含量造成氧化应激，对细胞DNA造成损伤。
Mycotoxins can affect cells growth, and result in oxidative stress through increase the generation of intracellular reactive oxygen species (ROS), causing DNA damage.
结论严重颅脑损伤后可出现明显的内毒素血症及炎性细胞因子反应，内毒素可能是引起和加重继发性脑损伤的原因之一。
Conclusion Obvious endotoxemia and inflammatory cytokine reaction may appear early in severe brain trauma. Endotoxin is likely one of the cause resulting in and aggravating secondary brain injury.
目的探讨内毒素血症时库普弗细胞激活对肝细胞损伤的作用机制。
ObjectiveTo study the roles of Kupffer cells activated by lipopolysaccharides (LPS) on rat primary cultured hepatocytes in endotoxemia.
结论内毒素诱导库普弗细胞释放的可溶性因子作用一定时间后可直接对肝细胞造成损伤。
ConclusionThe soluble factors released by Kupffer cells, which were activated by LPS, could cause direct hepatocytes injury.
结论内毒素诱导库普弗细胞释放的可溶性因子作用一定时间后可直接对肝细胞造成损伤。
ConclusionThe soluble factors released by Kupffer cells, which were activated by LPS, could cause direct hepatocytes injury.
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