The Role Of MicroRNA In The Acute Toxicity Of Rattus Induced By AFB1

Aflatoxins (AFT) are mycotoxins produced mainly by Aspergillus flavel and soon. Present, it is found that there are over twenty AFTs, and Aflatoxin B1(AFB1) isone of the ubiquitous and toxicant AFTs. AFB1can be found widely in improperlyfood and animal feeds. It is harmful not only to microbiologies and plants, but also tomammals.It may even cause cancers, such as hepatocelluar carcinoma(HCC).Thedamage is decided by both dose and time effect, and AFB1's major target organ isliver. Its long time effect may lead to tumor, and its short time effect will damge thecells,inhibit their proliferation or even induce apoptosis.Recent years, it is found thatmicroRNA (miRNA) is one kind of non-coding small RNAs,which is extremelyevolutionary conserved. It plays a key role not only in cell growth, development,differentiation and proliferation, but in the carcinoma genesis and metastasis. We aimto study the role of miRNA in the acute toxicity of rats induced by AFB1.In this study6rats were divided into two groups at random, each groupcontained three rats. The test and control group respectively received a single gastricintubation with AFB1and saline. The AFB1's dose was1.5mg/kg body weight.Threedays later,we found that the rats of test group eated less,moved slowly and shiveredsometimes. Their urine was yellow and their weight decreased. All of the rats werekilled after anesthesia by ether.Blood were collected to test liver function,It wasfound that lactic dehydrogenase (LDH), total bilirubin (TBI), alkaline phosphatase(ALP), Alanine aminotransferase (ALT) and glutamic oxaloacetic transaminase (AST)increased significantly. It showed that liver was impaired by AFB1. Then, the totalRNA of liver was extracted to conduct small RNA highthrough sequencing.Through the sequencing, we found there were116miRNA differentialexpression significantly, which included32up-regulation and84down-regualtion.Stem-loop RT-qPCR for miRNA vertified miR-34a was significantly up-regulated,confirming the result of highthroughput sequencing. At last, mimic miR-34a wastransfected into RH35cell, and it inhibited cell proliferation. So, miR-34a might playa role in the toxicity pathway induced by AFB1.