60-82-2Relevant articles and documents
Neuroprotective Effects of Trilobatin, a Novel Naturally Occurring Sirt3 Agonist from Lithocarpus polystachyus Rehd., Mitigate Cerebral Ischemia/Reperfusion Injury: Involvement of TLR4/NF-κB and Nrf2/Keap-1 Signaling
Chen, Nana,Gao, Jianmei,Gong, Qihai,Lei, Yaying,Li, Na,Shi, Jingshan,Wang, Wei,Xu, Fan
, p. 117 - 143 (2020)
Aims: Neuroinflammation and oxidative stress are deemed the prime causes of brain injury after cerebral ischemia/reperfusion (I/R). Since the silent mating-type information regulation 2 homologue 3 (Sirt3) pathway plays an imperative role in protecting against neuroinflammation and oxidative stress, it has been verified as a target to treat ischemia stroke. Therefore, we attempted to seek novel Sirt3 agonist and explore its underlying mechanism for stroke treatment both in vivo and in vitro. Results: Trilobatin (TLB) not only dramatically suppressed neuroinflammation and oxidative stress injury after middle cerebral artery occlusion in rats, but also effectively mitigated oxygen and glucose deprivation/reoxygenation injury in primary cultured astrocytes. These beneficial effects, along with the reduced proinflammatory cytokines via suppressing Toll-like receptor 4 (TLR4) signaling pathway, lessened oxidative injury via activating nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, in keeping with the findings in vivo. Intriguingly, the TLB-mediated neuroprotection on cerebral I/R injury was modulated by reciprocity between TLR4-mediated neuroinflammatory responses and Nrf2 antioxidant responses as evidenced by molecular docking and silencing TLR4 and Nrf2, respectively. Most importantly, TLB not only directly bonded to Sirt3 but also increased Sirt3 expression and activity, indicating that Sirt3 might be a promising therapeutic target of TLB. Innovation: TLB is a naturally occurring Sirt3 agonist with potent neuroprotective effects via regulation of TLR4/nuclear factor-kappa B and Nrf2/Kelch-like ECH-associated protein 1 (Keap-1) signaling pathways both in vivo and in vitro. Conclusion: Our findings indicate that TLB protects against cerebral I/R-induced neuroinflammation and oxidative injury through the regulation of neuroinflammatory and oxidative responses via TLR4, Nrf2, and Sirt3, suggesting that TLB might be a promising Sirt3 agonist against ischemic stroke.
Catalytic hydrogenation reaction of naringin-chalcone. Study of the electrochemical reaction
Nazareno,Giannuzzo,Mishima,Lopez De Mishima
, p. 589 - 590 (2000)
The electrocatalytic hydrogenation reaction of naringin derivated chalcone is studied. The reaction is carried out with different catalysts in order to compare with the classic catalytic hydrogenation.
METHODS FOR TREATING CHRONIC FATIGUE SYNDROME AND MYALGIC ENCEPHALOMYELITIS
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, (2021/03/13)
In one aspect the invention relates to a method of treatment selected from the group consisting of: (a) treating a symptom such as pain in a subject identified or diagnosed as having Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS); (b) treating a symptom such as pain in a subject having dysfunctional TRPM3 ion channel activity; (c) restoring NK cell function in a subject having dysfunctional TRPM3 ion channel activity; and (d) restoring calcium homeostasis in a subject having dysfunctional TRPM3 ion channel activity. The method comprises the step of administering to the subject a therapeutically effective amount of at least one therapeutic compound selected from the group consisting of: (i) an opioid receptor antagonist; (ii) an opioid antagonist; and (iii) a therapeutic compound that restores TRPM3 ion channel activity. In some embodiments the therapeutic compound is naltrexone hydrochloride.
Novel compound from plasma-treated phloridzin and anti-obesity composition comprising the same as effective component
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Paragraph 0039-0042, (2019/08/16)
The present invention relates to a novel compound derived from plasma-treated phloridzin and an anti-obesity composition comprising the same as an effective component and, more specifically, to a diameric compound derived from phloridzin, which is newly formed by plasma-treating phloridzin (methylene-bis-phloridzin, diglucosyl-methylene-bis-phloridzin, and methylene-bis-phloretin), and to an anti-obesity composition comprising the same as an effective component. In particular, the compound derived from phloridzin, comapred to phloridzin, inhibits the activity of pancreatic lipase and enhances the effect of suppressing fat accumulation during differentiation of fat cells. In particular, the methylene-bis-phloretin of the present invention, a diameric body formed by phloretin using a methyl group, a form of which sugars are removed from phloridzin, has excellent inhibitory effect on fat accumlation as compared to phloretin, and thus may be beneficially used as a material for anti-obesity therapeutic agents or anti-obesity functional health foods.COPYRIGHT KIPO 2019