肝移植大鼠肝窦内皮细胞细胞凋亡与移植肝肝细胞损害的关系

目的探讨冷保存肝移植大鼠肝窦内皮细胞（SEC）细胞凋亡与移植肝肝细胞损害的关系。方法雄性SD大鼠随机分为假手术组（n=6）、UW1h肝移植组（11=48）、UW12h肝移植组（n=48）。参照Kamada的方法行原位肝移植（OLT）。观察大鼠I68h存活率。分别于术后不同时相点采取血液及组织标本，检测血清丙氨酸氨基转移酶（ALT）及透明质酸（HA）水平；TUNEL法检测SEC凋亡，透射电镜观察细胞凋亡的形态学改变。结果UW12h组168h存活率为50％，显著低于UW1h组（F=6．39，P〈0．05）。UW12h组肝移植后血清ALT、HA水平明显高于UW1h组（F=3．99，P〈0．05；F=12．43，P〈0．05），两组大鼠ALT水平均于术后6h达高峰。UW12h组SEC凋亡指数（AI）明显高于UW1h组和假手术组（F值分别为63．58和86．58，P值均〈0．01），两组大鼠SEC的AI也于术后6h达高峰，与血中丙氨酸氨基转移酶（ALT）的高峰时相点一致。且两组大鼠SEC的AI均与ALT水平呈显著正相关（，值分别为1．0和0．962，P〈0．05）。结论SEC凋亡程度与移植肝肝细胞损害呈显著正相关，SEC凋亡是冷保存再灌注损伤的关锋环节。     

5-羟色胺2A受体阻断剂对大鼠肝脏再生的影响

目的观察5-羟色胺2A受体阻断剂酮色林对大鼠肝部分切除后肝再生的影响,了解5-羟色胺及其受体在肝脏再生中的作用。方法 80只雄性Wistar大鼠随机分为实验组和对照组。采用肝大部分切除术建立肝再生模型,术后16 h分别给予腹腔内注射酮色林（实验组）和生理盐水（对照组）,采用免疫组化及流式细胞技术动态观察并比较两组大鼠术后24、36、48、72 h肝脏Ki67、增殖细胞核抗原的表达情况。结果大鼠肝大部切除术后24、36 h肝脏表达Ki67、增殖细胞核抗原最为活跃,而后表达逐渐下降。实验组大鼠肝脏表达Ki67、增殖细胞核抗原较对照组显著下降（P〈0.05）。结论 5-羟色胺2A受体阻断剂酮色林显著抑制大鼠肝大部切除术后的肝脏再生,说明5-羟色胺具有一定的促进肝再生的作用,2A受体是其重要的信号传导受体之一。     

5-HT及其受体在大鼠肝再生过程中的作用

目的分析5-羟色胺（5-HT）及其受体在大鼠肝脏再生过程中的作用。方法将50只雄性Wistar大鼠随机分成实验组和对照组。实验组大鼠于肝大部分切除术后24、36、48和72h处死,对照组行假手术。采用流式细胞技术检测大鼠肝脏增殖细胞核抗原（PCNA）表达、免疫组化法检测Ki67及5-HT表达、实时荧光定量PCR检测5-HT2A、2B受体亚型的表达。结果肝大部切除术后大鼠肝脏重量逐渐增加,PCNA和Ki67表达于术后24和36h达高峰;在肝切除术后各个时间点5-HT2A、2B受体在肝脏中的表达均显著升高,以术后36h最高;术后36h空肠嗜铬细胞5-HT含量高于24h,且都高于正常大鼠。结论肝脏再生过程中5-HT合成及其受体表达均显著上调,可能与肝脏的再生有关。     

肝细胞生长因子对大鼠肝大部切除后再生的影响

目的：了解肝大部切除后再生过程中甲胎蛋白（AFP），端粒酶活性（TA），肝功能的变化，探讨肝细胞生长因子（HGF）治疗对肝细胞再生及AFP、TA、肝脏组织学、肝功能的影响。方法：选取体重200g左右大鼠24只并随机分成4组，其中组1进行肝大部切除后应用HGF治疗；组2仅进行肝大部切除部而不给予任何药物治疗；组3和组4均不进行切除手术，组3给予HGF治疗，组4则不给予任何治疗。1周后取材，再生肝组织TA采用PCR－ELISA法检测，AFP含量采用夹心ELISA法检测，另外，肝组织还作病理切片观察。结果：肝大部切除手术可使ALT明显升高（F＝8．01，P＜0．01），并可导致GGT增高（F＝9．71，P＜0．05）而使Alb降低（F＝6．28，P＜0．05），而HGF能显著降低ALT（F＝18．56，P＜0．01）和ALP（F＝6．28，P＜0．05），手术和HGF均可导致TA（F手术＝391．04，P＜0．01，FHGF＝29．59，P＜0．01）及AFP升高（F手术＝452．19，P＜0．01；FHGF＝8．23，P＜0．01）。组织病理学分析发现手术组的残肝和非手术组的肝脏大体组织形态学差异不大，手术对照组不论是再生肝还是残肝均有一定量的空泡变性，而手术组的再生肝则无典型的肝小叶结构，但可见肝窦，且细胞排列较残肝和非手术缓肝脏更密集，结论：HGF能显著促进肝细胞再生，有利于肝细胞膜的稳定性及肝功能的恢复。     

软肝煎对非酒精性脂肪肝大鼠肝纤维化的预防作用

目的：观察软肝煎对非酒精性脂肪肝大鼠肝纤维化的预防作用，并探讨其作用机制。方法：将38只SD大鼠随机分为4组，除正常组（N）外，其余3组即模型组（M）、软肝煎低剂量组（L）、软肝煎高剂量组（H）大鼠用高脂饲料喂养共16周，制备大鼠非酒精性脂肪肝模型。L组、H组大鼠以软肝煎低、高剂量灌胃，1次/d，共12周；N、M组大鼠以等量生理盐水灌胃。观察各组大鼠肝组织病理变化及TGF—β1阳性表达情况，检测血清PCⅢ、CⅣ、HA、LN水平，并进行比较。结果：M组大鼠肝组织呈脂肪变、炎性细胞浸润、肝细胞坏死、纤维组织明显增生，L、H组大鼠肝组织病理表现较M组明显减轻；M组大鼠TGF—β1阳性表达较N组增高（P〈0．05），而H组较M组则降低（P〈0.05）；M组大鼠各项血清学指标较N组明显升高（P〈0．05），而L、H组较M则明显降低（均P〈0．05），且此4项指标与肝纤维化存在正相关。结论：软肝煎不仅可以治疗脂肪肝、高脂血症，而且还具有确切地预防非酒精性脂肪肝纤维化作用。     

生长激素对鼠部分肝切除术后肝再生影响

目的　探讨生长激素对 70 %肝切除后肝再生的影响。方法　 60只SD大鼠随机分为对照组及生长激素组 ,按Higgins方法行 70 %肝切除术 ,术后给药并分批于术后 6、2 4、48、72、96h处死 ,作如下比较 :①残肝肝重 ;②增殖细胞核抗原 (PCNA)标记指数 ;③图像定量分析法测量PCNA阳性产物面积及灰度值。结果　与对照组比较 ,生长激素组残肝肝重、PCNA标记指数、PCNA阳性产物面积在术后均显著增高 (P <0 .0 5 ) ,而灰度值则显著降低 (P <0 .0 5 )。结论　生长激素具有强烈促进肝细胞增殖和刺激肝再生的作用     

细胞增殖与凋亡相关蛋白质在大鼠肝纤维化形成与消减中的动态变化

目的通过对四氯化碳诱导纤维化大鼠肝组织蛋白质组的分析，研究与增殖、凋亡相关蛋白质在肝纤维化过程中的动态变化，探讨细胞增殖与凋亡在肝纤维化形成及发展中的作用。方法将Wistao大鼠随机分为正常组、模型组。模型组大鼠皮下注射40％四氯化碳一橄榄油溶液，每周2次，共l2周，停止刺激后再观察4周。分别于第4、8、12、l6周末分批取材。留取肝组织分别做病理组织学、羟脯氨酸检查与蛋白质的分步提取。蛋白质定量后进行二维电泳，凝胶银染，用PDQUEST 2-DE图像分析软件对获得的蛋白质图谱进行分析，运用基质辅助激光解吸电离飞行时间质谱（MALDI—TOF—MS）鉴定30多个差异表达的蛋白质。结果从第1周开始模型组大鼠肝组织的胶原沉积、羟脯氨酸持续增高，在12周最高（P〈0．05），l6周下降（P〈0．05），各时间点模型组与正常组比较差异有统计学意义（P〈0．05）；模型组大鼠肝组织蛋白质组较正常组也有较大改变。经MALDI-TOF-MS鉴定与细胞增生相关的蛋白质或酶为：细胞增殖核抗原p120与p40、细胞周期蛋白F和泛素结合酶UBC7；与细胞凋亡相关的蛋白质主要有胱门蛋白酶12，只在模型组大鼠肝组织表达。结论与细胞增生、凋亡的相关蛋白质表达量在肝纤维化发生发展的不同阶段呈动态变化；在肝纤维化形成过程中细胞增生与凋亡受到相关蛋白质的调节。     

乳黄片对A型肝性脑病大鼠大脑皮层星形胶质细胞GFAP表达的影响

目的：探讨乳黄片对A型肝性脑病大鼠大脑皮层星形胶质细胞结构蛋白一神经胶质纤维酸性蛋白（CFAP）表达的影响。方法：Wistar雄性大鼠96只随机分为6组，正常对照组（A组）、模型组（B组）、乳果糖组（C组）、乳黄片低、中、高剂量组（D、E、F组）。除A组外，其余各组大鼠用硫代乙酰胺（TAA）造模，在TAA首次造模前，对A、B组大鼠灌以生理盐水1ml／100g。其余各组大鼠灌以相应药物。实验30小时后取材。免疫组化法测定大鼠皮层GFAP的表达水平。结果：B组大鼠GFAP染色阳性细胞以及平均光密度较A组明显降低，两者比较P〈0．01，差异有显著性意义。D、E、F组和C组大鼠GFAP均较B组显著升高（P〈0．01），且D、E、F组升高程度均较C组显著（P〈0．05或P〈0．01），其中以中剂量组升高最明显。结论：乳黄片有良好的防治A型肝性脑病的作用，其机制可能是通过保护肝细胞降低血氨进入血脑屏障的浓度，改善星形胶质细胞受损结构，提高GFAP蛋白表达而实现的。乳黄片抗A型肝性脑病的作用位点可能为星型胶质细胞。     

辨证治疗对非酒精性脂肪性肝病大鼠脂质过氧化及病理的影响

目的：探讨中医辨证治疗对非酒精性脂肪性肝病（NAFLD）大鼠肝脏脂质过氧化及病理影响。方法：取SPF级Wistar。大鼠72只，雌雄各半，随机分为正常组、模型组、对照药物治疗组、药物A方治疗组、药物B方治疗组，先A方后B方治疗组、先B方后A方治疗组、先空白后A方治疗组、先空白后B方治疗组，共9组。除正常组给予普通饲料外，其余各组大鼠饲以高脂饲料。造模第4周后，模型组加用等体积生理盐水灌胃；对照组加用对照药物灌胃；药物A方组加用治疗药物A方灌胃；药物B方组加用治疗药物B方灌胃；先A方后B方治疗组即4～8周用A方，8～12周用B方灌胃；先B方后A方治疗组即4～8周用B方，8～12周用A方灌胃；先空白后A方治疗组即先空白，第8～12周用A方灌胃；先空白后B方治疗组即先空白，第8～12周用B方灌胃。实验第12周时，测定大鼠肝组织SOD、MDA、GSH—ST的含量及评定大鼠肝组织脂肪变性程度及病理炎症活动度。结果：实验第12周时，先A方后B方治疗组提高NAFLD后期大鼠的肝组织SOD、GSH—ST含量的疗效与其他治疗组相比尤为显著（P〈0．01），降低脂质过氧化产物MDA含量的疗效显著（P〈0．01或尸〈0．05）；在对肝脏病理影响方面，先A方后B方治疗组减轻NAFLD后期大鼠肝细胞脂肪变，降低炎症活动度的疗效明显（P〈0．05或P〈0．01）。结论：在NAFLD的整个病程中，采取早期阶段运用疏肝健脾、活血化瘀、化痰利湿的治法，后期阶段运用化痰消瘀、清热利湿、补益肝肾治法的治疗方案，对于提高大鼠脂肪肝细胞抗氧化能力，降低脂质过氧化产物，减轻大鼠肝细胞脂肪变、降低炎症活动度的疗效显著优于其他治疗措施。     

重组人肝再生增强因子对大鼠肝部分切除后肝再生的影响

目的观察原核表达的重组人肝再生增强因子（rhALR）对大鼠肝再生的影响。方法按Higgins方法进行大鼠34％肝切除。术后4-6h各实验组大鼠经腹腔注射rhALR剂量分别为50μg、100μg、200μg、400μg、800μg,对照组给生理盐水。术后30h杀鼠取肝,增殖核抗原（PCNA）免疫组化染色和HE染色,进行肝细胞核PCNA阳性细胞计数和有丝分裂计数。结果rhALR能促进肝部分切除后大鼠肝细胞的有丝分裂和细胞核PCNA的表达,并呈现一定的剂量依赖关系。结论rhALR能促进在鼠肝再生和肝细胞增殖。     

The effect of ursodeoxycholic acid on liver regeneration after partial hepatectomy in rats with non-alcoholic fatty liver disease

Aim:  To investigate the effect of ursodeoxycholic acid (UDCA) on liver regeneration following partial hepatectomy in rats with non-alcoholic fatty liver disease (NAFLD).
Methods:  UDCA was administered to seven rats (group 1) and physiological saline was administered both to seven rats (group 2) with NAFLD and to seven rats with normal livers (group 3). All rats underwent two-thirds hepatectomy and the remnant liver tissues were removed 48 h later. Mitotic index (MI) and levels of proliferating cell nuclear antigen (PCNA), glutathione (GSH) and malondialdehyde (MDA) were assayed.
Results:  MI and PCNA levels in group 2 were significantly lower than in groups 1 and 3, but the values in groups 1 and 3 were similar. The GSH levels of group 2 were significantly lower than those of group 3 in the hepatectomy tissues, and lower than those of groups 1 and 3 in the remnant tissues. The differences between GSH levels in groups 1 and 3 were not significant. MDA levels in hepatectomy and remnant tissues were significantly higher in group 2 compared to groups 1 and 3; values in groups 1 and 3 were similar.
Conclusion:  UDCA increases regeneration after partial hepatectomy in rats with NAFLD, possibly due to an attenuating effect on oxidative stress.     

Effect of vascular endothelial growth factor on hepatic regenerative activity following partial hepatectomy in rats.

BACKGROUND/AIMS: Vascular endothelial growth factor (VEGF) is an angiogenic factor with a growth-promoting effect that is thought to be restricted to vascular endothelial cells. Its essential role during liver regeneration has yet to be determined. The aim of this study was to document the effect of exogenous VEGF administration on liver regeneration in rats undergoing submaximal hepatic resections. METHODS: Adult male Sprague-Dawley rats (n = 4/group) undergoing 30% partial hepatectomy were administered 200 ng VEGF165 intravenously and were sacrificed at 24, 36, and 48 h postoperatively. Liver regeneration was monitored by measuring the restituted liver mass, proliferating cell nuclear antigen (PCNA) immunostaining, and hepatic PCNA protein by Western blot. RESULTS: Changes in restituted liver mass 48 h postsurgery were more prominent, but did not differ statistically between VEGF-treated and control rats (47% vs. 29%; p<0.06). Nevertheless, PCNA immunostaining showed increased labeling index of hepatocytes, apparent at 36 and 48 h after partial hepatectomy (38% vs. 18% [p<0.041 and 42% vs. 11% [p<0.021], respectively). Hepatic PCNA proteins measured by Western blot showed a 3-fold increase in VEGF-treated rats 48 h postsurgery compared with controls (p<0.01). CONCLUSION: Exogenous VEGF administration early after partial hepatectomy stimulates liver regeneration in rats. Whether or not VEGF165 is a direct mitogen for hepatocytes remains to be determined.     

Ischemic preconditioning improves liver regeneration by sustaining energy metabolism after partial hepatectomy under ischemia in rats.

BACKGROUND: The protective effect of ischemic preconditioning (IPC) has been reported on improvement of survival, reduction of liver necrosis and enhancement of the regenerative capacity of hepatocytes after partial hepatectomy. This study was undertaken to confirm that IPC has a significant impact on regeneration of hepatocytes after partial hepatectomy in ischemically damaged liver. In addition, we sought to examine the role of adenine nucleotides in this process. METHODS: Wistar rats were subjected to 60 min of total hepatic ischemia, followed by 70% hepatectomy. The animals were subdivided into an IPC (10/15 min) group and a non-IPC (control) group. Liver function tests and arginase activity were analyzed. Hepatic adenosine triphosphate (ATP), adenosine diphosphate and adenosine monophosphate were measured using gradient high-performance liquid chromatography. The liver regeneration was identified using relative liver weight and proliferating cell nuclear antigen (PCNA) labeling index. RESULTS: IPC treatment improved serum liver enzymes and tissue arginase activity (P<0.05) when compared with the control group. The preconditioned livers were associated with upregulation of ATP expression and also increased tissue energy charge. Regenerated liver weight in the IPC group was significantly higher than in the control group (P<0.05). The PCNA labeling index in the remnant livers in the IPC group was also significantly increased at 24 and 48 h after partial hepatectomy (P<0.05). CONCLUSION: These results suggest that IPC-augmented liver regeneration after hepatectomy, probably due to the stabilization of energy metabolism in rats.     

普罗布考对大鼠非酒精性脂肪性肝病的预防及机制研究

目的 观察普罗布考对大鼠非酒精性脂肪性肝病（NAFLD）的预防作用．并探讨其可能作用机理。方法 24只雄性sD大鼠随机分3组：正常对照组、NAFLD对照组、普罗布考干预组。以高脂饲料饲养诱发脂肪肝大鼠模型。18周末，处死所有动物，检测血脂、肝功能、肝脂质含量、氧化还原指标、肝组织病理学等。结果与NAFLD对照组比较，普罗布考干预组TC（2．98±0．90）mmol／L vs（4．45±1．15）mmol／L，ALT（78．25±18．47）U／L vs（110．2±36．33）U／L及肝组织TG含量（2．61±0．20）mmol／L vs（2．93±0．36）mmol／L均显著下降（P均〈0．05），其肝脂肪变性及炎症程度亦显著减轻（P均〈0．05）。结论 普罗布考可对高脂饲料饲养诱发的大鼠NAFLD产生保护作用；其保护作用与提高机体抗氧化能力．减轻组织氧化应激损害有关。     

Improvement of the survival rate after rat massive hepatectomy due to the reduction of apoptosis by caspase inhibitor

BACKGROUND AND AIM: Acute liver failure after massive hepatectomy is caused by both necrosis and apoptosis in the remnant liver. We investigate the protective effect of the caspase inhibitor on apoptosis after massive hepatectomy in rats. METHODS: Benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (ZVAD-fmk) is a general inhibitor of the caspase. Male Wister rats weighing 200-300 g were divided into three groups: 90Hx group undergoing 90% hepatectomy, 95Hx group undergoing 95% hepatectomy, 95Hx + ZVAD group undergoing 95% hepatectomy and administration of ZVAD-fmk. The 7-day survival rate was studied, and the rats were sacrificed at the 1, 2, 3, 5, and 7th day after hepatectomy. The remnant liver tissues were stained with hematoxylin-eosin, and with proliferating cell nuclear antigen (PCNA) for evaluation of liver regeneration, and with TdT-mediated dUTP-biotin nick end labeling (TUNEL) and in situ oligo ligation method (ISOL) for evaluation of apoptosis. RESULTS: The 7-day survival rates were 100%, 0%, and 30%, in the 90Hx, 95Hx, and 95Hx + ZVAD groups, respectively. There was no significant difference in PCNA labeling index (LI) between the 95Hx and 95Hx + ZVAD groups. TUNEL and ISOL LI of 95Hx + ZVAD group were significantly lower than those of 95Hx group. Fatal liver failure after massive hepatectomy was characterized by more apoptosis and less mitosis of hepatocytes. ZVAD-fmk could significantly attenuate apoptosis of hepatocytes in the remnant liver and improve the survival rate after 95% hepatectomy in rats. CONCLUSION: Caspase inhibitors such as ZVAD-fmk may provide a new adjuvant therapy to treat liver failure after massive hepatectomy.     

Failure of regeneration of the steatotic rat liver: disruption at two different levels in the regeneration pathway

Hepatic resection or transplantation in patients with fatty liver is associated with increased morbidity and mortality. The regenerative capacity of fatty livers after major tissue loss is unknown. Interleukin 6 (IL-6) is a potent inducer of hepatic regeneration in normal and ischemic livers. Therefore, we studied hepatic regeneration at day 1, day 2, and day 4 in a model of 70% hepatectomy in obese and lean Zucker rats, and obese Zucker rats pretreated with recombinant interleukin 6 (rIL-6). The mitotic cycle in hepatocytes was investigated by 4 different markers of regeneration representing distinct phases of mitosis (proliferating cell nuclear antigen [PCNA] = G(1) phase, bromodeoxy uridine [BrdU] = S phase, mitotic index, and regenerated liver weight = M phase). Obese Zucker rats had significantly decreased regenerative capacity compared with lean Zucker rats (PCNA, BrdU, mitotic index, regenerated liver weight) at days 1 and 2 after surgery. Four days after resection fatty animals showed an increase in the mitotic index indicating a delay of regeneration in steatotic livers. Animal survival after 70% hepatectomy was significantly decreased in obese rats compared with lean animals. Pretreatment of obese animals with rIL-6 normalized PCNA expression (G(1) phase) in steatotic hepatocytes but failed to increase DNA synthesis (BrdU, S phase), mitosis (mitotic index and regenerated liver weight, M phase), and animal survival. These results indicate major impairment of hepatic regeneration in steatotic livers. Two different blockages of regeneration must be present, one rIL-6 sensitive, at the level of IL-6 or upstream, and a second, rIL-6 resistant, at the level of G(1)/S-phase transition.     

Appearance of an inhibitory cell nuclear antigen in rat and human serum during variable degrees of hepatic regenerative activity

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Mild hypothermia does not affect liver regeneration after partial hepatectomy in mice

Background: The use of mild hypothermia has been suggested to be therapeutically useful in treating acute liver failure. It is not known if hypothermia influences liver regeneration. Aim: To assess the effect of hypothermia on liver regeneration in mice. Methods: After partial (70%) hepatectomy (PHx), C57BL6/J mice were randomly assigned to either a hypothermic group or a normothermic group. Controlled mild hypothermia was maintained for up to 3 h after surgery. In addition, assessment of liver mass restitution was examined by studying the induction of key cell cycle proteins (cyclin A, D1 and E) and hepatocyte proliferation [assessment of proliferating cell nuclear antigen (PCNA) protein expression] by Western blotting and DNA synthesis by measuring 5‐bromo‐2‐deoxyuridine (BrdU) incorporation by immunohistochemical techniques 45 h after PHx. Results: Partial hepatectomy induced a vigorous proliferative response in the remnant livers of both groups of mice (normothermic and hypothermic groups), as evidenced by the induction of key cyclins, PCNA and incorporation of BrdU after PHx. The liver/body weight ratio and both cyclin and PCNA protein expression as well as BrdU incorporation did not differ between the regenerating livers of hypothermic and normothermic groups. Conclusion: Mild hypothermia does not influence liver regeneration in mice.     

Hepatic ratio of phosphatidylcholine to phosphatidylethanolamine predicts survival after partial hepatectomy in mice

A major predictor of failed liver resection and transplantation is nonalcoholic fatty liver disease (NAFLD). NAFLD is linked to a wide spectrum of diseases including obesity and diabetes that are increasingly prevalent in Western populations. Thus, it is important to develop therapies aimed at improving posthepatectomy outcomes in patients with NAFLD, as well as to improve the evaluation of patients slated for hepatic surgery. Decreased hepatic phosphatidylcholine (PC) content and decreased ratio of hepatic PC to phosphatidylethanolamine (PE) have previously been linked to NAFLD. To determine if decreased hepatic PC/PE could predict survival after hepatectomy, we used mouse models lacking key enzymes in PC biosynthesis, namely, phosphatidylethanolamine N-methyltransferase and hepatic-specific CTP:phosphocholine cytidylyltransferase α. These mice were fed a high-fat diet to induce NAFLD. We then performed a 70% partial hepatectomy and monitored postoperative survival. We identified hepatic PC/PE to be inversely correlated with the development of steatosis and inflammation in the progression of NAFLD. Decreased hepatic PC/PE before surgery was also strongly associated with decreased rates of survival after partial hepatectomy. Choline supplementation to the diet increased hepatic PC/PE in Pemt(-/-) mice with NAFLD, decreased inflammation, and increased the survival rate after partial hepatectomy. Conclusion: Decreased hepatic PC/PE is a predictor of NAFLD and survival following partial hepatectomy. Choline supplementation may serve as a potential therapy to prevent the progression of NAFLD and to improve postoperative outcome after liver surgery.