Chang of Plasma Interleukin-18, Interleukin-10and Interleukin-18/Interleukin-10Ratio in Rats with Non-alcoholic Fatty Liver Disease

Background and Objective:Increased with the improvement of people’s living quality,improved the structure of the food, the aging of the population andthe progress of the disease monitoring method, NAFLD has become themost common clinical liver disease at developed area of our countrycoastal city. At the onset of foreign adult rate reached20%-33%,75%-90%and morbid obesity,3%-5%will develop more nonalcoholicfatty hepatitis, cirrhosis and hepatocellular carcinoma.Aprospective study of20years of follow-up, approximately20%ofpatients with NASH in5-10years to progress to cirrhosis. Obesityprevalence of NASH was60%-75%, the prevalence of NAFLD in patientswith type2diabetes mellitus is50%-70%. The United States in88cases of patients with polycystic ovary syndrome complicated withNAFLD55%. With age, gender, diagnosis criteria of region, racevaries with the growth of the age, the prevalence of NAFLD firstincreased and then decreased, the prevalence rate of male was higherthan female, Hispanic NAFLD prevalence rate is higher than theordinary people, African Americans low prevalence;In recent years,the incidence of NAFLD in China after the rate of viral hepatitis,become China’s second largest liver disease, but its pathogenesis is not completely clear. The present study proposed " two strike "or " theory of multiple hit " doctrine, insulin resistance (InsulinResistance, IR) caused by the first blow lead to fat deposition inthe liver, by oxidative stress and lipid peroxidation caused byinflammatory reaction on the basis of the second the disease strikes.The two together cause the occurrence and development of NAFLD. Butits mechanism is still not clear, while seeking a fast method toestablish an animal model of NAFLD is now urgent research hot spot。Interleukin18(interleukin-10, IL-18) is a proinflammatorycytokine, plays an important role in inflammatory reaction;interleukin10(interleukin-10, IL-10) is an anti-inflammatorycytokine important, dynamic change between the two can reflect theinflammatory reaction in a certain extent. The possible mechanismof this experiment is to○1by high fat diet, construction of NAFLDanimal model and to clarify the high fat diet induced NAFLD;○2Tocalculate the serum IL-18, IL-10, IL-18/IL-10of NAFLD rats and toexplain its relationship with fatty liver rats in the correlationbetween IL-18and IL-10,○3To explain IL-18/IL-10and liver tissueinflammatory changes, above three of purposes to explain IL-18, IL-10,IL-18/IL-10in the pathogenesis of NAFLD possible role and clinicalsignificance.Methods:By high fat diet to establish NAFLD animal model; The serumof TG and FBS measured by enzyme method by automatic biochemicalinstrument at Affiliated Hospital of Guilin Medical College; by enzyme-linked immunosorbent assay (ELISA) method for thedetermination of IL-18, IL-10and IL-18/IL-10ratios were calculatedby determination of thiosulfate; MDA, deacidification method;pathological tissue sections were stained with HE after theobservation of NAFLD rat liver fat and inflammatory changes in theelectron microscope.Results:The model group compared with normal group, the liver index,FBS, TG, MDA increased significantly (P<0.05); under electronmicroscope, obvious inflammation and liver steatosis; NAFLD modelgroup rats serum IL-18, IL-18/IL-10levels were significantly higherthan that of the normal group and the ratio of IL-10is lower thanthat of normal group (P <0.05), and IL-18and the degree ofinflammation related (r=0.71, P<0.05), IL-10, IL-18/IL-10ratioand the degree of inflammation and steatosis degree of correlation(r=-0.64, P <0.05; r=-0.46, P <0.05; R=0.70, P <0.05; R=0.61, P<0.05).Conclusions:1By high fat diet maybe construct a NAFLD rat animal model;2The NAFLD model group of rat IL-18and IL-18/IL-10increase，whileIL-10decrease；3The group of NAFLD rats serum IL-18, IL-10and IL-18/IL-10levelsand the degree of inflammation, fatty change has certaincorrelation.