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Diverse Pharmacological Activities and Potential Medicinal Benefits of Geniposide Hindawi Evidence-Based Complementary and Alternative Medicine Volume 2019, Article ID 4925682, 15 pages https://doi.org/10.1155/2019/4925682 Review Article Diverse Pharmacological Activities and Potential Medicinal Benefits of Geniposide Yan-Xi Zhou,1,2 Ruo-Qi Zhang,1 Khalid Rahman ,3 Zhi-Xing Cao,1 Hong Zhang ,4 and Cheng Peng 1 1 Pharmacy College, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China 2Library, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China 3School of Pharmacy and Biomolecular Sciences, Faculty of Science, Liverpool John Moores University, Liverpool L3 3AF, UK 4Institute of Interdisciplinary Medical Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China Correspondence should be addressed to Hong Zhang; [email protected] and Cheng Peng; [email protected] Received 2 January 2019; Accepted 19 March 2019; Published 16 April 2019 Academic Editor: Jairo Kennup Bastos Copyright © 2019 Yan-Xi Zhou et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Geniposide is a well-known iridoid glycoside compound and is an essential component of a wide variety of traditional phytomedicines, for example, Gardenia jasminoides Elli (Zhizi in Chinese), Eucommia ulmoides Oliv. (Duzhong in Chinese), Rehmannia glutinosa Libosch. (Dihuang in Chinese), and Achyranthes bidentata Bl. (Niuxi in Chinese). It is also the main bioactive component of Gardeniae Fructus, the dried ripe fruit of Gardenia jasminoides Ellis. Increasing pharmacological evidence supports multiple medicinal properties of geniposide including neuroprotective, antidiabetic, hepatoprotective, anti-infammatory, analgesic, antidepressant-like, cardioprotective, antioxidant, immune-regulatory, antithrombotic, and antitumoral efects. It has been proposed that geniposide may be a drug or lead compound for the prophylaxis and treatment of several diseases, such as Alzheimer’s disease, Parkinson’s disease, diabetes and diabetic complications, ischemia and reperfusion injury, and hepatic disorders. Te aim of the present review is to give a comprehensive summary and analysis of the pharmacological properties of geniposide, supporting its use as a medicinal agent. 1. Introduction diseases, such as Alzheimer's disease (AD), Parkinson’s dis- ease (PD), diabetes and diabetic complications, ischemia and Geniposide (C17H24O10; Figure 1), a well-known iridoid gly- reperfusion injury, and hepatic disorders. Te aim of the coside compound, is one of the main bioactive components present review is to give a comprehensive summary and of traditional Chinese medicine Gardeniae Fructus, the dried analysis of the pharmacological properties of geniposide, ripe fruit of Gardenia jasminoides Ellis (Zhizi in Chinese). supporting the potential uses of geniposide as a medicinal It has been isolated and identifed in nearly 40 species of agent. plants and most of which are medicinal herbs [1]. Over the past few decades, there has been a rapid growth in the 2. Pharmacology Actions information available on the pharmacological activities of geniposide. Studies have shown that geniposide displays a 2.1. Anti-Alzheimer’s Disease Activity. AD is the most com- wide spectrum of in vitro and in vivo pharmacological efects, mon neurodegenerative disorder of progressive cognitive including neuroprotective, antidiabetic, hepatoprotective, decline in the aged population [2]. A number of stud- anti-infammatory, analgesic, antidepressant-like, cardiopro- ies have demonstrated the anti-AD activity of geniposide tective, antioxidant, immune-regulatory, antithrombotic, and both in vitro and in vivo. Formaldehyde is neurotoxic, and antitumoral efects (summarized in Table 1), and these phar- long-term overdose increases the risk of AD. An increase macological efects lay the foundation for geniposide of being in the concentration of endogenous formaldehyde in the a potential therapeutic agent for the treatment of several brain has been found to correlate with dementia in aging 2 Evidence-Based Complementary and Alternative Medicine OH at 25 mg/kg for 3 months signifcantly inhibited RAGE- HO O mediated signaling, lowered the production of TNF-� and � � O IL-1 , and suppressed cerebral A accumulation. Moreover, O geniposide ameliorated learning and memory defcits [8]. HO O O A large body of evidence indicates that insulin-degrading enzyme (IDE) plays an essential role in the degradation of A�. Geniposide enhanced the expression of IDE in primary cor- HO tical neurons, and this efect was reversed by LY294002 (an OH inhibitor for phosphatidyl inositol 3-kinase, PI3K), GW9662 Figure 1: Chemical structure of geniposide. (an antagonist for peroxisome proliferator-activated receptor �,PPAR�), AG1478 (an antagonist for epidermal growth factor receptor), H89 (an inhibitor for protein kinase A, PKA), and PP1 (an inhibitor for c-Src). Furthermore, it people. In human neuroblastoma SH-SY5Y cells, treatment upregulated the phosphorylation of PPAR� and promoted with geniposide at a concentration of 100 �Mameliorated the release of phosphorylated FoxO1 from nuclear fraction the morphology of formaldehyde- (0.12 mM) injured cells. to the cytosol. In addition, geniposide directly activated the Furthermore, geniposide increased the production of the activity of IDE promoter in PC12 cells [9]. In neuroblastoma antiapoptotic gene Bcl-2 at both mRNA and protein levels, SH-SY5Y cells, incubation with geniposide at 1 and 10 �M while decreasing the expression of the proapoptotic gene P53, for 24 h notably augmented the level of IDE protein in a apoptotic executer caspase-3, and apoptotic initiator caspase- concentration-dependent manner [10]. 9. Moreover, geniposide elevated the activity of intracellular Furthermore, an increasing number of studies have antioxidants, including superoxide dismutase (SOD) and demonstrated that leptin has protective efect against AD. � glutathione peroxidase (GSH-Px) [3]. Incubation of murine Geniposide treatment inhibited the level of A 1-42 both in rat N2a neuroblastoma cells with formaldehyde (0.09 mM) for 24 primary cortical neurons (10 �M) and in APP/PS1 transgenic h notably changed cell morphology, decreased cell viability, mice (10, 20, and 40 mg/kg, i.g.). Moreover, geniposide at and promoted apoptosis, and these efects were reversed by 10 �M induced the phosphorylation of Janus kinase 2 and supplementation with geniposide (200 �M). In particular, signal transducer and activator of transcription 3 (STAT3), geniposide remarkably ameliorated morphology and cell upregulated the protein level of ADAM10, and downregulated numbers, increased cell viability, upregulated the expression the expression of BACE1 in rat primary cortical neurons, of Akt and Bcl-2, and lowered the expression of FoxO3 and and these efects were reversed by the preincubation with p53 [4]. leptin antagonist (50 ng/mL) [11]. Formation of intracellular Amyloid plaques composed of insoluble amyloid-� (A�) neurofbrillary tangle from hyperphosphorylated tau is one deposits are a characteristic pathological feature of AD and of the typical hallmark lesions of AD as well. Administration A� aggregated with oligomer is known to be able to induce of geniposide enhanced the expression of leptin receptor and cellular toxicity as well as cognitive impairment. Incubation diminished the phosphorylation of tau both in rat primary with geniposide at 83.8 �M reduced the cytotoxicity of cultured cortical neurons in vitro and in APP/PS1 transgenic A� (10 �M) in rat hippocampal neurons and promoted mice in vivo. Additionally, geniposide at 10 �Minducedthe the outgrowth of neurites both in their length and in the phosphorylation of Akt at Ser-473 site and glycogen synthase dendrite number per neuron. Geniposide at 5, 100, and kinase-3� (GSK-3�) at Ser-9 site in primary cultured cortical 200 �M increased the cell viability of SY5Y-APP695sw cells neurons, and this efect of geniposide on Akt and GSK-3� treated with A�42 aggregates. Furthermore, geniposide at 100 as well as the efect of geniposide on tau phosphorylation �M promoted fbrillogenesis and increased the formation could be inhibited by leptin antagonist (50 nM) [12]. Treat- of high molecular masses of A�42 polymers, resulting in a ment with geniposide for 4 weeks also attenuated insulin decrease of the quantity and cytotoxicity of A�42 oligomers defciency-induced phosphorylated level of tau and acceler- [5]. Moreover, geniposide averted A�1−42-induced cell injury ation of GSK-3� phosphorylation in the brain of APP/PS1 in primary cultured cortical neurons [6]. Te receptor for transgenic mice. It also augmented the efect of insulin on advanced glycation end products- (RAGE-) mediated signal- the phosphorylation of tau, Akt, and GSK-3� in primary ing pathway is related to A�-induced pathogenic responses. cultured cortical neurons, and these efects were reversed by Geniposideat50,100,and200�M suppressed RAGE- LY294002 [13]. In streptozotocin- (STZ-) induced AD model mediated signaling (activation of extracellular regulated pro- rats, injection of geniposide at 50 �M to the lateral ventricle tein kinase (ERK) 1/2 and inhibited kappa B (I�B)/nuclear reduced STZ-induced spatial learning defcit, tau phospho- factor-�B(NF-�B)) and attenuated the production of tumor rylation, and GSK-3� hyperactivity. Additionally, it inhibited necrosis factor-� (TNF-�) and interleukin-1�
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