Effect Of Endurance Swimming On Hepatocytes Apoptosis In The Process Of High-Fat Diet Induced NASH In Rats

Nonalcoholic fatty liver disease (nonalcoholic fatty liver disease, NAFLD) is oneof the major diseases of modern civilization, and serious harmful to human health.The prevalence of NAFLD is approximately20~30percent and grows rapidly all ofthe world.NAFLD is becoming one of the most common liver diseases.Hepatocyteapoptosis plays an important role in the process of NASH formation, there is a closerelationship between hepatocyte apoptosis and liver inflammation.Therefore, it canimprove liver inflammation and prevent NASH by reducing the hepatocyte apoptosisthrough various means.Objective: To observe the effect of different stages of endurance swimming onserum FFA, TNF-alpha and express of apoptosis-related proteins in the high-fat dietrats.And discuss the role of exercise on hepatocyte apoptosis and liver inflammationin the process of NASH.It will provide a theoretical basis for prevention andimprovement of NASH by exercise.Methods:84Sprague-Dawley (SD) male rats were randomly assigned into twogroups: standard diet group and high-fat diet group.Each group is divided into twosubgroups, sedentary group and training group and total of four groups.Standard dietsendently Group (Group C), Standard diet training group (group E), High-fat dietsendently Group (Group H), high-fat diet training group (Group HE). The meterialswas collected in4weeks,8weeks and12weeks after training. Observinghepatohistological sections and evaluating theseverity of steatosis and histologicalactivity index (HAI), Western blot method was used for caspase-3, bcl-2and baxprotein expression; flow cytometry was used for hepatocyte apoptosisResults:(1)Average daily caloric intake: All experimental stages, the average dailycalorie intake of H groups were higher than C groups (p<0.01), E groups were lowerthan C groups (p<0.01), HE groups were higher than E groups (p<0.01), HE groupswere lower than the H groups (p<0.01). (2) Body weight and liver weight: At the experiment stages of4weeks and12weeks, the body weight of H groups were higher than C groups (p<0.01); At theexperiment stages of8weeks and12weeks, E groups were lower than C groups(p<0.05),HE groups were lower than H groups (p<0.05)All experimental stages,theliver weight of H groups were higher than C groups (p<0.01), HE groups were higherthan E groups (p<0.01) and group HE12was lower than group H12(p<0.05).(3) Serum parameter: All experimental stages, serum FFA of H groups werehigher than C groups (p<0.05), HE groups were lower than H groups (p<0.05); In8weeks and12weeks, E groups were lower than C groups (p<0.01), and group HE12was lower than group E12(p<0.05). Serum ALT of group H12was higher than groupC12(p<0.01). Serum levels of TNF-alpha of group H12was higher than group C12(p<0.01), group HE12was lower than group H12(p<0.01).(4) Hepatocyte apoptosis index: All experimental stages, hepatocyte apoptosisindex of H groups were higher than C groups (p<0.01); Exercise can increase the rateof hepatocyte apoptosis in H groups, and group HE12was lower than group H12(p<0.01).(5) Liver apoptosis related proteins: Liver caspase-3and bax protein expressionshowed that group H8was higher than group C8(p<0.01); group H12was higher thangroup C12(p<0.01), group HE12was higher than group E12(p<0.01), group E12waslower than group C12(p<0.05), group HE12was lower than group H12(p<0.01).Liver Bcl-2protein expression showed that group H4was lower than groupC4(p<0.05), group HE4was lower than group C4(p<0.05); and group H8was lowerthan group C8(p<0.01), group HE8was higher than group H8(p<0.01); group H12was lower than group C12(p<0.01), group E12was higher than group C12(p<0.05),group HE12was higher than group H12(p<0.01), group HE12was lower than groupE12(p<0.01).(6) Hepatic steatosis degree and hepatic inflammatory activity score: Hepaticsteatosis results showed that, all experimental stages,the hepatic steatosis degree of Hgroups were higher than C groups(p<0.01), HE groups were higher than E groups(p<0.01), and H groups were higher than HE groups (p<0.01); group H12was higher than group HE12(p=0.068). Each experimental stage,liver inflammation activity scoreshowed that C groups were lower than H groups(p<0.01); and group HE8was lowerthan group H8(p=0.055), group HE12was lower than group H12(p<0.01).Conclusions:(1)12-week high-fat diet can successful induce NASH model, the mechanismmay be that high-fat diet can increase serum FFA and increase hepatic lipid in livercells and promote liver inflammation reaction;(2) Endurance swimming can effectively alleviate the development of high-fatdiet induced NASH in rats and improve its symptoms. The mechanism may be thatexercise can limit the calorie intake of rats, reduce blood serum and provent thelipid accumulation in liver cells, and it can provent the NASH process and reduceliver inflammation by declining hepatocyte apoptosis;(3) Hepatocyte apoptosis may be an important reason for high-fat diet inducedNASH and it can promote the development of simple hepatic steatosis to NASH.