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Genipin & Tissue Engineering

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Genipin & Tissue Engineering

Product Abstract:

Genipin CAS 6902-77-8 is extracted from gardenia fruit.The white crystal is a kind of new material for tissue engineering.

Product Description



[CAS No.]?6902-77-8

[Original]: Dry fruits of Gardenia Jasminoides Ellis

[Appearance]:White powder or crystalline.


  1. It will slowly yellowing when exposure to air long term.
  2. The inhibition of Gastric function was anticholinergic, it’s the strongest substances which can inhibit the mutagenic activity of the mutagen among the ever found iridoid glycosides.
  3. Soluble in ethanol, acetone, chloroform, diethyl ether, etc.; slightly soluble in water.
  4. Melting point:120--122°C.

Application: Genipin & Tissue Engineering

Sun W, Incitti T, Migliaresi C, Quattrone A, Casarosa S, Motta A. Genipin-crosslinked gelatin-silk fibroin hydrogels for modulating the behaviour of pluripotent cells. J Tissue Eng Regen Med. 2014 Jan 29. doi: 10.1002/term.1868.


Different hydrogel materials have been prepared to investigate the effects of culture substrate on the behaviour of pluripotent cells. In particular, genipin-crosslinked gelatin-silk fibroin hydrogels of different compositions have been prepared, physically characterized and used as substrates for the culture of pluripotent cells. Pluripotent cells cultured on hydrogels remained viable and proliferated. Gelatin and silk fibroin promoted the proliferation of cells in the short and long term, respectively. Moreover, cells cultured on genipin-crosslinked gelatin-silk fibroin blended hydrogels were induced to an epithelial ectodermal differentiation fate, instead of the neural ectodermal fate obtained by culturing on tissue culture plates. This work confirms that specific culture substrates can be used to modulate the behaviour of pluripotent cells and that our genipin-crosslinked gelatin-silk fibroin blended hydrogels can induce pluripotent cells differentiation to an epithelial ectodermal fate



Qi L, Cui X, Dong W, Barrera R, Coppa GF, Wang P, Wu R.

Ghrelin Protects Rats Against Traumatic Brain Injury and Hemorrhagic Shock Through Upregulation of UCP2. Ann Surg. 2014 Mar 25. [Epub ahead of print]


OBJECTIVE: To determine the mechanism responsible for ghrelin's neuroprotective effects after traumatic brain injury (TBI) and hemorrhagic shock.

BACKGROUND:: Ghrelin, a gastrointestinal hormone, has been demonstrated to possess multiple functions, including upregulation of uncoupling protein 2 (UCP2) and stimulation of the vagus nerve. Recent evidence has indicated that ghrelin is neuroprotective. We, therefore, hypothesized that ghrelin protects rats against TBI and hemorrhagic shock through upregulation of UCP2, involving stimulation of the vagus nerve.

METHODS: Brain injury was induced by dropping a 450 g of weight from 1.5 m onto a steel helmet attached to the skull of male adult rats. Immediately after TBI, a midline laparotomy was performed, and both lumbar veins were isolated and severed at the junction with the vena cava. The abdomen was kept open for 20 minutes. At 45 minutes after TBI and uncontrolled hemorrhage (UH), ghrelin (4, 8, or 16 nmol/rat) or 1 mL of normal saline (vehicle) was intravenously administered. The Neurological Severity Scale (NSS), morphological alterations and β-amyloid precursor protein expression in the brain, systemic organ injury markers (ie, alanine aminotransferase, aspartate aminotransferase, and lactate), and UCP2 expression in the cortex were measured. To determine whether the protective effect of ghrelin is mediated through upregulation of UCP2, genipin, a specific UCP2 antagonist, was administered intravenously before the injection of ghrelin in animals with TBI and UH. The role of the vagus nerve was assessed by performing vagotomy immediately before ghrelin administration.

RESULTS: Ghrelin attenuated brain injury and facilitated functional recovery after TBI and UH. Ghrelin increased UCP2 expression in the cortex, and administration of genipin abolished ghrelin's protection after TBI and UH. Furthermore, vagotomy prevented the beneficial effects of ghrelin and eliminated ghrelin-induced UCP2 upregulation after TBI and UH.

CONCLUSIONS: The protective effects of ghrelin after TBI and UH seem to be related to upregulation of UCP2 expression in the brain and requiring the intact vagus nerve.


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