Nolan J P
Hepatology. 1981 Sep-Oct;1(5):458-65. doi: 10.1002/hep.1840010516.
The concept that relates intestinal bacteria and their toxins as a common pathway of liver injury by toxic agents has interested investigators for a long period. Recently, a number of studies in experimental animals and in patients with liver disease support this contention, and are reviewed. Evidence is presented to suggest that: (a) function of the sinusoidal cells is critical to integrity of the hepatocyte; (b) damage to these lining cells by several agents may be the initial injury leading to decreased ability of the liver to detoxify endotoxin (LPS); (c) following this primary injury to Kupffer and endothelial cells, LPS causes damage at amounts which are ordinarily innocuous and may represent a final pathway of liver necrosis; (d) "spillover" of LPS may lead to systemic manifestations of liver disease, and (e) modification of endotoxin toxicity or absorption may protect against several acute and chronic liver injuries.
肠道细菌及其毒素作为毒性物质导致肝损伤的共同途径这一概念，长期以来一直吸引着研究人员。最近，一些针对实验动物和肝病患者的研究支持了这一观点，并在此进行综述。有证据表明：(a) 肝血窦细胞的功能对肝细胞的完整性至关重要；(b) 多种因素对这些内衬细胞的损伤可能是导致肝脏对内毒素（LPS）解毒能力下降的初始损伤；(c) 在库普弗细胞和内皮细胞受到这种原发性损伤后，LPS在通常无害的剂量下即可造成损伤，这可能是肝坏死的最终途径；(d) LPS的“溢出”可能导致肝病的全身表现，以及 (e) 对内毒素毒性或吸收的改变可能预防多种急慢性肝损伤。
