Prostaglandin E2 promotes hepatic bile acid synthesis by an E prostanoid receptor 3‐mediated hepatocyte nuclear receptor 4α/cholesterol 7α‐hydroxylase pathway in mice

Yan, Shuai; Tang, Juan; Zhang, Yuyao; Wang, Yuanyang; Zuo, Shengkai; Shen, Yujun; Zhang, Qianqian; Chen, Di; Yu, Yu; Wang, Kai; Duan, Sheng‐Zhong; Yu, Ying

doi:10.1002/hep.28928

Cited by 16 publications

(12 citation statements)

References 52 publications

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“…Primary mouse hepatocytes were isolated from 8-to 12-week-old mice using a two-step collagenase-perfusion technique as described previously (21). Hepatocytes were cultured in DMEM supplemented with 25 mmol/L glucose, 10% FBS, and 50 mg/mL penicillin and streptomycin at 37°C and 5% CO 2 /95% air.…”

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

Prostaglandin F2α Facilitates Hepatic Glucose Production Through CaMKIIγ/p38/FOXO1 Signaling Pathway in Fasting and Obesity

et al. 2018

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Gluconeogenesis is drastically increased in patients with type 2 diabetes and accounts for increased fasting plasma glucose concentrations. Circulating levels of prostaglandin (PG) F are also markedly elevated in diabetes; however, whether and how PGF regulates hepatic glucose metabolism remain unknown. Here, we demonstrated that PGF receptor (F-prostanoid receptor [FP]) was upregulated in the livers of mice upon fasting- and diabetic stress. Hepatic deletion of the FP receptor suppressed fasting-induced hepatic gluconeogenesis, whereas FP overexpression enhanced hepatic gluconeogenesis in mice. FP activation promoted the expression of gluconeogenic enzymes (PEPCK and glucose-6-phosphatase) in hepatocytes in a FOXO1-dependent manner. Additionally, FP coupled with G in hepatocytes to elicit Ca release, which activated Ca/calmodulin-activated protein kinase IIγ (CaMKIIγ) to increase FOXO1 phosphorylation and subsequently accelerate its nuclear translocation. Blockage of p38 disrupted CaMKIIγ-induced FOXO1 nuclear translocation and abrogated FP-mediated hepatic gluconeogenesis in mice. Moreover, knockdown of hepatic FP receptor improved insulin sensitivity and glucose homeostasis in / mice. FP-mediated hepatic gluconeogenesis via the CaMKIIγ/p38/FOXO1 signaling pathway, indicating that the FP receptor might be a promising therapeutic target for type 2 diabetes.

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Section: Cell Culture and Treatmentsmentioning

confidence: 99%

Prostaglandin F2α Facilitates Hepatic Glucose Production Through CaMKIIγ/p38/FOXO1 Signaling Pathway in Fasting and Obesity

et al. 2018

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“…The central analgesic activity could have been due to inhibition of the nociceptive effects of noradrenaline, bradykinin, prostaglandins, adrenaline, adenosine, serotonin, and acetylcholine. On the other hand, the peripheral analgesic effect could be attributed to inhibition of the discharge of endogenous pain mediators like prostaglandin-2 (PGE 2) and PGE 2 -α in peritoneal fluids including lipoxygenase which triggers the nociceptive neurons (24).…”

Section: Discussionmentioning

confidence: 99%

Analgesic potential of dichloromethane leaf extracts of Eucalyptus globulus (Labill) and Senna didymobotrya (Fresenius) in mice models

Mworia

Kibiti

Ngeranwa

et al. 2020

J Herbmed Pharmacol

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Introduction: Pain is managed using conventional drugs like paracetamol, aspirin and diclofenac among others. Synthetic drugs have many side effects. This study aimed at evaluating the analgesic potential of the dichloromethane leaf extracts of Eucalyptus globulus and Senna didymobotrya in mice. Methods: The dichloromethane leaf extracts of E. globulus and S. didymobotrya were subjected to quantitative phytochemical analysis using gas chromatography-mass spectrophotometry (GC-MS). In vivo analgesic evaluation comprised of nine groups of animals (Swiss albino mice): normal, positive, negative control and six experimental groups that received 25, 50, 100, 150, 200 and 250 mg/kg body weight of each plant extract intraperitoneally. Thirty minutes later, they were injected with 0.01 mL of 2.5% formalin. The animals in positive control group were administered diclofenac (15 mg/kg) and formalin, the normal control mice received 3% dimethyl sulfoxide (DMSO) in normal saline, while the negative group received DMSO in normal saline and formalin. All the doses were administered intraperitoneally. The duration of shaking and licking of the injected paw was scored and analyzed. Results: The analysis revealed that E. globulus contained alpha-pinenes, endo-fenchol, α-eudesmol, myrcene, camphene, alpha-phellandrene, limonene, and camphor while S. dymobotrya possessed camphene, alpha-phellandrene, limonene, and camphor. In the late phase, E. globulus at the doses of 25, 50, 100, 150, 200 and 250 mg/kg reduced the paw licking time by 34.03%, 60.79%, 84.33 %, 90.65%, 94.49%, 98.52%, respectively while S. didymobotrya extract reduced the paw licking time by 26.48%, 32.96%, 87.04%, 91.27%, 93.40%, 90.97%, and 96.82%, respectively. Conclusion: The results of this study validate and support the traditional uses of these plants as analgesics.

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“…Global Ep3 deletion promotes to diet-induced obesity and exaggerates ectopic lipid deposition such as in skeletal muscle in mice3940. Hepatic Ep3 deficiency exacerbated atherosclerosis in hyperlidemic mice through suppression of biliary cholesterol secretion in mice41. However, Ep3 mediates vasoconstriction42, and genetic deletion of Ep3 receptor increases bleeding tendency38 and reduces atherosclerosis-related thrombosis43, suggesting Ep3 involvement in platelet activation.…”

Section: Discussionmentioning

confidence: 99%

Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

et al. 2017

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Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6Clow and Ly6Chigh) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E2 is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6Clow Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFβ1 signalling and subsequently inhibits Ly6Clow Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6Clow Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI.

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Prostaglandin E2 promotes hepatic bile acid synthesis by an E prostanoid receptor 3‐mediated hepatocyte nuclear receptor 4α/cholesterol 7α‐hydroxylase pathway in mice

Cited by 16 publications

References 52 publications

Prostaglandin F2α Facilitates Hepatic Glucose Production Through CaMKIIγ/p38/FOXO1 Signaling Pathway in Fasting and Obesity

Prostaglandin F2α Facilitates Hepatic Glucose Production Through CaMKIIγ/p38/FOXO1 Signaling Pathway in Fasting and Obesity

Analgesic potential of dichloromethane leaf extracts of Eucalyptus globulus (Labill) and Senna didymobotrya (Fresenius) in mice models

Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

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