|Source:||The fruit of Gardenia jasminoides Ellis.|
|Biological Activity or Inhibitors:||1. Geniposidic acid has anti-atherosclerotic effects, can protect vascular endothelium and reverse plaque formation in an atherosclerotic model.
2. Geniposidic acid and geniposide have antitumor effects, they play a role in an effective anticancer product with the ability to decrease undesirable radiation damage to the hematologic tissue after high dose irradiation.
3. Geniposidic acid can protect against D-galactosamine and lipopolysaccharide-induced hepatic failure in mice.
4. Geniposidic acid protects against anti-induced hepatotoxity and acute intrahepatic cholestasis, due to Fxr-mediated regulation of Bsep and Mrp2.
5. Geniposidic acid has effects on the expression of MRP2 and BSEP in BRL-3A cells after FXR gene silencing mediated by si RNA.
|Solvent:||DMSO, Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.6717 mL||13.3583 mL||26.7165 mL||53.4331 mL||66.7913 mL|
|5 mM||0.5343 mL||2.6717 mL||5.3433 mL||10.6866 mL||13.3583 mL|
|10 mM||0.2672 mL||1.3358 mL||2.6717 mL||5.3433 mL||6.6791 mL|
|50 mM||0.0534 mL||0.2672 mL||0.5343 mL||1.0687 mL||1.3358 mL|
|100 mM||0.0267 mL||0.1336 mL||0.2672 mL||0.5343 mL||0.6679 mL|
Pharm Biol. 2015 Feb;53(2):280-5.
|Anti-atherosclerotic effect of geniposidic acid in a rabbit model and related cellular mechanisms.[Pubmed: 24963945]|
|Compared with the model control group, the plaque area, intima/media thickness ratio, and intimal foam cells number in Geniposidic acid (80, 160, and 240 mg/kg) subgroups were significantly improved (p < 0.05). By HE staining, the activities of Geniposidic acid on relieving ECs shedding and improving aortic morphology disorders were also demonstrated. From the results of CCK-8 testing, only 100 μg/ml Geniposidic acid performed significant inhibition on SMC proliferation. The relative IC50 of Geniposidic acid on SMC inhibition was 87.73 μg/ml. Geniposide acid also showed promotion effect on ECs proliferation, and the related ED50 of Geniposidic acid was 86.05 μg/ml. Besides, only 50 and 100 μg/ml Geniposidic acid showed obvious inhibition on SMC migration from the upper chamber (p < 0.05). DISCUSSION AND CONCLUSION: The effects of Geniposidic acid on protecting vascular endothelium and reversing plaque formation in an atherosclerotic model were demonstrated.|
Cancer Lett. 1997 Feb 26;113(1-2):31-7.
|Comparisons of geniposidic acid and geniposide on antitumor and radioprotection after sublethal irradiation.[Pubmed: 9065798]|
|The antitumor effects of two iridoid compounds, Geniposidic acid (GA) and geniposide (GP), were investigated in mice along with their possible effects on radioprotection after sublethal X-irradiation. Decreases in the growth of the implanted tumor by ascitic cells were a result of intraperitoneal administration of GA and GP at high concentrated levels. This result was achieved by exerting the levels of dosage in a dose-dependent manner. Except on the 12th day after treatment by the dosage of 500 mg/kg, reduced radiation effects of mice treated with the drugs in the 30 min preirradiated period by GA and GP on peripheral leukocytes were not observed significantly by the sublethal whole-body X-irradiation. And except on the 7th day after treatment, when these two compounds were administered i.p. to mice 30 min before 4 Gy irradiation, neither GA nor GP enhanced significantly the postirradiation responses of splenic blastogenesis by PHA. In addition, GA might be a more potent tumor growth inhibitor than GP when combined with the X-irradiation, though there was no significant synergetic effect on their combined antitumor activity. The preliminary results of GA and GP on hematological and blastogenic observations in this study suggested that they may very well, partially, play a role in an effective anticancer product with the ability to decrease undesirable radiation damage to the hematologic tissue after high dose irradiation.|
J Ethnopharmacol. 2013 Mar 7;146(1):271-7.
|Geniposidic acid protects against D-galactosamine and lipopolysaccharide-induced hepatic failure in mice.[Pubmed: 23298456]|
|ETHNOPHARMACOLOGICAL RELEVANCE: Geniposidic acid (GA) is an iridoid glucoside isolated from Gardeniae jasminoides Ellis (Rubiaceae) that has long been used to treat inflammation, jaundice and hepatic disorders. AIMS OF THE STUDY: This study examined the cytoprotective properties of Geniposidic acid against D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant hepatic failure. MATERIALS AND METHODS: Mice were given an intraperitoneal injection of Geniposidic acid (12.5, 25, 50 mg/kg) 1h before receiving GalN (800 mg/kg)/LPS (40 μg/kg). Liver and blood samples were collected 1 and 8 h after GalN/LPS injection. RESULTS: The survival rate of the Geniposidic acid group was significantly higher than the control. GalN/LPS increased serum aminotransferase activity, serum tumor necrosis factor-α level and hepatic lipid peroxidation and decreased hepatic glutathione content. These changes were attenuated by Geniposidic acid. Geniposidic acid augmented increases in serum interleukin-6 level, heme oxygenase-1 and NF-E2-related factor 2 protein expression. Mice treated with Geniposidic acid decreased cleaved caspase-8 and caspase-3 protein expression and showed significantly fewer apoptotic cells. Geniposidic acid increased Bcl-xL protein expression and decreased Bax protein expression. Moreover, Geniposidic acid treatment enhanced phosphorylation of signal transducer and activator of transcription 3. CONCLUSION: Our findings suggest that Geniposidic acid alleviates GalN/LPS-induced liver injury by enhancing antioxidative defense system and reducing apoptotic signaling pathways.|
China Journal of Traditional Chinese Medicine & Pharmacy, 2016,5.
|Effects of geniposidic acid on the expression of MRP2 and BSEP in BRL-3A cells after FXR gene silencing mediated by si RNA[Reference: WebLink]|
|To investigate the effects of Geniposidic acid(GPA) on the protein expression of multidrug resistance protein 2(MRP2) and bile salt export pump(BSEP) in BRL-3A cells, which was mediated by small interfering RNA(si RNA) farnesoid X receptor(FXR) gene silencing. Methods: RT-PCR was used to detect the result of FXR gene silencing and the gene levels of FXR, MRP2 and BSEP in BRL-3A cells affected by GPA, and Western blot was used to detect whether FXR gene silencing in BRL-3A cells or not by GPA and the protein expressions of FXR, MRP2 and BSEP in BRL-3A cells induced by Geniposidic acid. Results: Compared with control group, the levels of m RNA and protein expressions of FXR, MRP2 and BSEP in BRL-3A cells were significantly increased in GPA group with the concentration of 4mmol/L and 1mmol/L(P0.01, P0.05). GPA with concentration of 4mmol/L and 1mmol/L could significantly reverse the levels of m RNA and protein expression of FXR, MRP2 and BSEP in BRL-3A cells(P0.01, P0.05), which was mediated by si RNA-FXR. Conclusion: FXR gene silencing could down-regulate the levels of m RNA and protein expression of MRP2 and BSEP, and the GPA could up-regulate FXR to upregulate the levels of m RNA and protein expression of MRP2 and BSEP.|
J Ethnopharmacol. 2016 Feb 17;179:197-207.
|Geniposidic acid protected against ANIT-induced hepatotoxity and acute intrahepatic cholestasis, due to Fxr-mediated regulation of Bsep and Mrp2.[Pubmed: 26723467]|
|Some abnormalities were observed on ANIT treated rats including weight loss, reduced food intake and hair turned yellow. Obtained results demonstrated that at dose 100 and 50mg/kg B.W. (P<0.01) and 25mg/kg B.W. (P<0.05) of Geniposidic acid (GPA) pretreated dramatically prevented ANIT induced decreased in bile flow rate. Compared with ANIT treated group, the results of bile biochemical parameters about total bile acid (TBA) was increased by GPA at groups with any dose (P<0.01), glutathione (GSH) was increased significantly at high dose (P<0.01) and medium dose (P<0.05), total bilirubin (TB) was increased at high and medium dose (P<0.05), direct bilirubin (DB) was only increased at high dose (P<0.01). Serum levels of glutamic-Oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), γ-glutamyltranspeptidase (γ-GT), TB, DB and TBA in comparison with ANIT treated group (P<0.01) were reduced by GPA (between 100 and 50mg/kg B.W.) pretreatment. Histopathology of the liver tissue showed that pathological damages and hepatic portal area filled with bile were relieved after GPA pretreatment compared with ANIT treated group. The protein and mRNA expression of Fxr, Bsep and Mrp2 were decreased in ANIT treated group. On the contrary, the protein and mRNA of Fxr, Bsep and Mrp2 were up regulated significantly pretreatment by GPA at dose of high and medium groups. On protein level of Bsep and Mrp2 the result shown no statistical difference in GPA (25mg/kg B.W.), but it was not same shown in mRNA level. CONCLUSION: The results of this investigation have demonstrated that the GPA exerts a dose dependent hepatoprotection effect on ANIT induced liver damage with acute intrahepatic cholestasis in rats, which may due to Fxr mediated regulation of bile transporters like Bsep and Mrp2.|