4,5‐dicaffeyolquinic acid improves high‐fat diet‐induced cognitive dysfunction through the regulation of insulin degrading enzyme

Kang, Jin Yong; Park, Seon Kyeong; Kim, Jong Min; Park, Su Bin; Yoo, Seul Ki; Han, Hye Ju; Kim, Dae‐Ok; Heo, Ho Jin

doi:10.1111/jfbc.12855

Cited by 8 publications

(8 citation statements)

References 36 publications

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“…According to research by Kang et al. (2019), MDA content increased when HFD was given to mice for 16 weeks. HFD affects antioxidant systems by reducing SOD, GSH and CAT activities.…”

Section: Discussionmentioning

confidence: 99%

“…ROS generated by HFD may lead to lipid peroxidation in the brain and liver (Matsumoto & Takekawa, 2014). According to research by Kang et al (2019), MDA content increased when HFD was given to mice for 16 weeks. HFD affects antioxidant systems by reducing SOD, GSH and CAT activities.…”

Section: Discussionmentioning

confidence: 99%

“…A mouse received an electric shock when it entered a dark area (0.5 mA and 2 s once). After 24 hr, the time for the mouse to enter the dark segment was measured for 5 min maximum (Kang et al., 2019).…”

Section: Methodsmentioning

confidence: 99%

“…After that, the supernatant was mixed with 0.65 N NaOH, 0.26 M tris–HCl buffer (pH 7.8) and o‐phthalaldehyde (OPT) reacted in the dark. After 15 min, it was measured at 320 nm excitation and 420 nm emission filters using a fluorescence microplate reader (Infinite F200, Tecan Co., San Jose, CA, USA) (Kang et al., 2019).…”

Section: Methodsmentioning

confidence: 99%

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Ameliorative effect of persimmon ( Diospyros kaki ) in cognitively impaired diabetic mice

et al. 2020

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Insulin resistance induced by the excessive consumption of a highfat diet is known to cause metabolic syndromes such as type 2 diabetes mellitus (T2DM). Insulin resistance, characterized as one of the symptoms of T2DM, induces hyperglycemia by inhibiting glucose uptake into cells and maintaining high glucose levels in the blood (Dong et al., 2016). A sustained hyperglycemic state promotes the production of reactive oxygen species (ROS) and it can disrupt the antioxidant system of brain and liver tissue (Li et al., 1999). The produced ROS is related to lipid peroxidation of brain, kidney and liver. In particular, because brain tissue has a high content of unsaturated

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“…According to research by Kang et al. (2019), MDA content increased when HFD was given to mice for 16 weeks. HFD affects antioxidant systems by reducing SOD, GSH and CAT activities.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Ameliorative effect of persimmon ( Diospyros kaki ) in cognitively impaired diabetic mice

et al. 2020

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“…The abundant phytochemical components in plants, such as polyphenols and flavonoids, can relieve inflammation and treat related diseases, based on which various drugs have been developed [ 11 , 12 ]. Among these, chlorogenic acid and mono- and dicaffeoyl esters of quinic acid have attracted attention because of their antioxidant, antiviral, antibacterial, and anticancer activities [ 12 , 13 , 14 , 15 ]. The structure of dicaffeoylquinic acid (diCQA) contains two caffeic acid molecules linked to one quinic acid molecule via an ester bond.…”

Section: Introductionmentioning

confidence: 99%

Anti-Inflammatory Effect of 4,5-Dicaffeoylquinic Acid on RAW264.7 Cells and a Rat Model of Inflammation

et al. 2021

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Anti-inflammatory agents that are safer and more effective than the currently used non-steroidal anti-inflammatory drugs are urgently needed. The dicaffeoylquinic acid (diCQA) isomer 4,5-diCQA exhibits antioxidant activity and various other health-promoting benefits; however, its anti-inflammatory properties require further investigation. This study was conducted to evaluate the anti-inflammatory properties of 4,5-diCQA in vitro and in vivo using RAW264.7 cells and a carrageenan-induced inflammation model, respectively. In RAW264.7 cells, 4,5-diCQA pretreatment significantly inhibited lipopolysaccharide-induced expression of nitric oxide, prostaglandin E2, nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, interleukin-1β, and interleukin-6, without inducing cytotoxicity. The inhibitory effects of 4,5-diCQA were mediated by the suppression of nuclear factor-κB nuclear translocation and mitogen-activated protein kinase (MAPK) phosphorylation. Oral administration of 4,5-diCQA at doses of 5, 10, and 20 mg/kg of the body weight suppressed carrageenan-induced edema and the expression of nitric oxide synthase, cyclooxygenase-2, and tumor necrosis factor-α in a dose-dependent manner. Collectively, our results suggest that 4,5-diCQA exerts anti-inflammatory effects by suppressing activation of the nuclear factor-κB and MAPK pathways in vitro and reducing carrageenan-induced edema in vivo. Therefore, 4,5-diCQA shows potential as a natural alternative to non-steroidal anti-inflammatory drugs.

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Dipeptidyl Peptidase 4 (DPP4) Exacerbates Osteoarthritis Progression in an Enzyme‐Independent Manner

Li,

Zhang,

Jiang

et al. 2024

Advanced Science

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Chondrocyte senescence is a key driver of osteoarthritis (OA). Mitochondrial dysfunction and oxidative stress can induce chondrocyte senescence. However, the specific mechanisms by which senescence contributes to OA progression are not fully understood. Here, it is attested that Dipeptidyl peptidase 4 (DPP4) is significantly upregulated in osteoarthritic chondrocytes in both humans and mice. DPP4 promotes oxidative stress and cellular senescence in chondrocytes through excessive mitochondrial fission in an enzyme‐independent manner. Intra‐articular injection of adeno‐associated virus 2 to upregulate DPP4 in chondrocytes promotes post‐traumatic and aging‐induced OA in mice in an enzyme‐independent manner. Mechanistically, DPP4 competitively binds to Myosin heavy chain 9 (MYH9), interfering with its E3 ubiquitin ligase Carboxyl terminus of Hsc70‐interacting protein (CHIP), and thereby upregulates MYH9 expression. Finally, a small molecule, 4,5‐Dicaffeoylquinic acid is identified, which disrupts the interaction between DPP4 and MYH9, thereby ameliorating post‐traumatic and aging‐induced OA in mice caused by DPP4 upregulation. The study indicates that the non‐enzymatic activity of DPP4 is a promising target for OA treatment.

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4,5‐dicaffeyolquinic acid improves high‐fat diet‐induced cognitive dysfunction through the regulation of insulin degrading enzyme

Cited by 8 publications

References 36 publications

Ameliorative effect of persimmon ( Diospyros kaki ) in cognitively impaired diabetic mice

Ameliorative effect of persimmon ( Diospyros kaki ) in cognitively impaired diabetic mice

Anti-Inflammatory Effect of 4,5-Dicaffeoylquinic Acid on RAW264.7 Cells and a Rat Model of Inflammation

Dipeptidyl Peptidase 4 (DPP4) Exacerbates Osteoarthritis Progression in an Enzyme‐Independent Manner

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