Synergistic neuroprotective effects of Geniposide and ursodeoxycholic acid in hypoxia‑reoxygenation injury in SH‑SY5Y cells

Cheng, Fang; Ma, Chongyang; Sun, Lingxiao; Zhang, Xiaoyu; Zhai, Changming; Li, Changxiang; Zhang, Shuang; Ren, Beida; Liu, Shilin; Liu, Songnan; Yin, Xiangjun; Wang, Xueqian; Wang, Qingguo

doi:10.3892/etm.2017.5395

Cited by 13 publications

(12 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Autophagy activation, ERS, and oxidative stress play significant roles in the development of cerebral I/R injury [106, 107]. Treatment with a combination of geniposide and tauroursodeoxycholic acid could counteract the elevation in cellular ROS levels, the activation of oxygen-glucose deprivation-reoxygenation- (OGD/R-) induced ERS, and autophagy in SH-SY5Y cells with hypoxia-reoxygenation injury [108]. On the other hand, inflammatory events that occur between the blood-endothelium interface of the cerebral capillaries also underlie the resultant ischemic tissue damage [109].…”

Section: Preclinical Evidence For the Therapeutic Potential Of Genmentioning

confidence: 99%

Antioxidative Property and Molecular Mechanisms Underlying Geniposide-Mediated Therapeutic Effects in Diabetes Mellitus and Cardiovascular Disease

et al. 2019

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Geniposide, an iridoid glucoside, is a major component in the fruit of Gardenia jasminoides Ellis (Gardenia fruits). Geniposide has been experimentally proved to possess multiple pharmacological actions involving antioxidative stress, anti-inflammatory, antiapoptosis, antiangiogenesis, antiendoplasmic reticulum stress (ERS), etc. In vitro and in vivo studies have further identified the value of geniposide in a spectrum of preclinical models of diabetes mellitus (DM) and cardiovascular disorders. The antioxidative property of geniposide should be attributed to the result of either the inhibition of numerous pathological processes or the activation of various proteins associated with cell survival or a combination of both. In this review, we will summarize the available knowledge on the antioxidative property and protective effects of geniposide in DM and cardiovascular disease in the literature and discuss antioxidant mechanisms as well as its potential applications in clinic.

show abstract

Section: Preclinical Evidence For the Therapeutic Potential Of Genmentioning

confidence: 99%

Antioxidative Property and Molecular Mechanisms Underlying Geniposide-Mediated Therapeutic Effects in Diabetes Mellitus and Cardiovascular Disease

et al. 2019

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Besides this, geniposide was revealed to be beneficial in suppressing Helicobacter pylori infections [10]. Moreover, the neuroprotective effects of geniposide were observed in diverse cells like SH-SY5Y and PC12 to against oxygen and glucose deprivation-evoked damage [11,12]. That interests us to conduct an in vitro study to explore the effects of geniposide on SCI.…”

Section: Introductionmentioning

confidence: 99%

Geniposide protects PC12 cells from lipopolysaccharide-evoked inflammatory injury via up-regulation of miR-145-5p

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

Geniposide is an active ingredient with anti-apoptotic and anti-inflammatory properties. This study was to examine the effects of geniposide on a cell model of spinal cord injury (SCI). PC12 cells were administrated with geniposide before subjected to LPS. The effects of geniposide were analyzed by utilizing CCK-8 assay, apoptosis assay, ELISA, RT-qPCR and Western blot. We found that PC12 cells viability was unchanged by treating with geniposide. However, geniposide with concentrations of 200 or 300 lg/mL significantly mitigated LPS-evoked viability loss. Meanwhile, apoptosis driven by LPS was mitigated by geniposide, which accompanied with p53, Bax and cleaved caspase-3 down-regulation, and Bcl-2 up-regulation. Besides this, the expression and release of IL-1b, IL-6, IL-8 and TNF-a evoked by LPS were mitigated by geniposide. miR-145-5p was a target of geniposide. miR-145-5p expression was up-regulated by geniposide, and geniposide did not protect PC12 cells against LPS injury when miR-145-5p was silenced. Moreover, geniposide inhibited NF-jB and JNK pathways via up-regulating miR-145-5p. In short, the present work described the neuroprotective effects of geniposide by targeting miR-145-5p. Further mechanisms involved in geniposide's beneficial effects are correlated with the inhibited NF-jB and JNK pathways. HIGHLIGHTS 1. Geniposide prevents LPS-induced injury in PC12 cells; 2. Geniposide up-regulates miR-145-5p; 3. Geniposide protects PC12 cells via up-regulation of miR-145-5p; 4. Geniposide inhibits NF-jB and JNK pathways via up-regulation of miR-145-5p.

show abstract

“…PERK is a critical transmembrane signaling protein ( 35 ), and eIF-2α is a key protein in the PERK pathway ( 36 ). TUDCA is a neuroprotective drug via inhibiting ER stress ( 37 ). We found that TUDCA reversed the decline in the expression of GluR1, PSD95, and CREB.…”

Section: Discussionmentioning

confidence: 99%

Cognitive Impairment and Endoplasmic Reticulum Stress Induced by Repeated Short-Term Sevoflurane Exposure in Early Life of Rats

et al. 2018

View full text Add to dashboard Cite

Sevoflurane is one of the most commonly used volatile anaesthetics for children, but the safety of prolonged or repeated clinical use of sevoflurane in infants or children is controversial. Here, we investigated the effects of sevoflurane on rats in early life and the time scale of those effects. Our behavioral results indicated that repeated short-term exposure of new-born rats to sevoflurane caused learning and memory impairment, while a single exposure of rats to sevoflurane was relatively safe. Further mechanistic investigation revealed that repeated sevoflurane exposure impaired long-term potentiation (LTP), downregulated the expression of certain synaptogenesis-related proteins (GluR1, PSD95) and upregulated proteins related to endoplasmic reticulum (ER) stress in the hippocampus. An ER stress inhibitor, tauroursodeoxycholic acid (TUDCA), reversed the changes in the levels of synaptic plasticity proteins. Our results provide new evidence for the clinical concerns regarding repeated sevoflurane anesthesia.

show abstract

Synergistic neuroprotective effects of Geniposide and ursodeoxycholic acid in hypoxia‑reoxygenation injury in SH‑SY5Y cells

Cited by 13 publications

References 26 publications

Antioxidative Property and Molecular Mechanisms Underlying Geniposide-Mediated Therapeutic Effects in Diabetes Mellitus and Cardiovascular Disease

Antioxidative Property and Molecular Mechanisms Underlying Geniposide-Mediated Therapeutic Effects in Diabetes Mellitus and Cardiovascular Disease

Geniposide protects PC12 cells from lipopolysaccharide-evoked inflammatory injury via up-regulation of miR-145-5p

Cognitive Impairment and Endoplasmic Reticulum Stress Induced by Repeated Short-Term Sevoflurane Exposure in Early Life of Rats

Contact Info

Product

Resources

About