Precautions of Chenodeoxycholic Acid:1. Careful when using this function without the gallbladder. 2. The goods for dissolution therapy requires a certain period, it should be used in stationary phase cholelithiasis, and cholangitis should not be used often or recently occurred complications such as pancreatitis or cholecystitis. 3. Chronic liver disease, liver and kidney function is not normal, peptic ulcer, inflammatory bowel disease, uncontrolled hypertension, coronary sclerosis, pathological obesity, liver toxicity, and recently used drugs, are not FDA should. 4. This product is taking a longer period, which normally takes six months or even more than a year, can play a role in dissolving gallstones. 5. Studies have shown that the product of the fetal rhesus potential liver toxicity, so pregnant women should be avoided, and pregnancy increases the saturation of bile into the stone and nature, it will affect the efficacy.
Detailed test methods are as follows: HepG2 cells were treated with chenodeoxycholic acid (CDCA) ± ω3PUFA. Activation of PPARα was evaluated, and expression of PPARα, farnesoid X receptor (FXR), liver X receptor alpha (LXRα), and retinoid X receptor (RXR) mRNA was evaluated by RT-PCR.  PPARα activation was increased in HepG2 cells treated with ω3PUFA, and decreased in the presence of CDCA when compared to untreated cells. PPARα mRNA was reduced by 67% with CDCA and restored to the level of control with ω3PUFA. LXRα mRNA increased 2-fold with CDCA treatment and was significantly reduced by ω3PUFA.
Expression of PPARα, as well as LXRα mRNA levels, were reduced with Chenodeoxycholic Acid(CDCA) treatment and restored with the addition of ω3PUFA. These results suggest PPARα and LXRα may be mediators by which ω3PUFA attenuate bile acid-induced hepatocellular injury.  Omega-3 long-chain polyunsaturated fatty acids (ω3PUFA) have been shown to be anti-inflammatory in the attenuation of hepatocellular injury. Peroxisome proliferator-activated receptor alpha (PPARα) is a nuclear receptor transcription factor that inhibits the activation of NFκB, thereby repressing inflammation, and ωPUFA are PPARα ligands. The purpose of this study was to determine if ω3PUFA 
attenuate bile acid-induced apoptosis via PPARα.