Neuroprotective effects of phenolic glycosides from Populus tomentiglandulosa roots in HT22 mouse hippocampal neuronal cells

Kim, Soeun; Lee, Phil Jun; Fang, Bo; Park, Seon Ju; Saravanakumar, Kandasamy; Irfan, Navabshan; Pham, Chau Ha; Yoo, Gayoung; Yoo, Hee Min; Cho, Namki

doi:10.1016/j.molstruc.2022.134685

Cited by 3 publications

(4 citation statements)

References 39 publications

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“…Excessive glutamate can cause neuronal cell death by increasing apoptotic protein levels, such as Bax, cytochrome c, caspase-9, and caspase-3, while decreasing anti-apoptotic protein levels, including Bcl-2 [ 35 , 41 , 42 , 43 ]. To further illustrate the effect of AHE on glutamate-induced apoptosis, the protein expressions of apoptotic markers, including Bax, Bcl-2, cytochrome c, and cleaved caspase-9, were determined using Western blot analysis.…”

Section: Resultsmentioning

confidence: 99%

Neuroprotective Effects of Albizia lebbeck (L.) Benth. Leaf Extract against Glutamate-Induced Endoplasmic Reticulum Stress and Apoptosis in Human Microglial Cells

et al. 2023

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Endoplasmic reticulum (ER) stress caused by excessive glutamate in the central nervous system leads to neurodegeneration. Albizia lebbeck (L.) Benth. has been reported to possess neuroprotective properties. We aimed to investigate the effect and mechanism of A. lebbeck leaf extracts on glutamate-induced neurotoxicity and apoptosis linked to ER stress using human microglial HMC3 cells. A. lebbeck leaves were extracted using hexane (AHE), mixed solvents, and ethanol. Each different extract was evaluated for cytotoxic effects on HMC3 cells, and then non-cytotoxic concentrations of the extracts were pretreated with the cells, followed by glutamate. Our results showed that AHE treatment exhibited the highest protective effect and was thus selected for finding the mechanistic approach. AHE inhibited the specific ER stress proteins (calpain1 and caspase-12). AHE also suppressed the apoptotic proteins (Bax, cytochrome c, cleaved caspase-9, and cleaved caspase-3); however, it also increased the antiapoptotic Bcl-2 protein. Remarkably, AHE increased cellular antioxidant activities (SOD, CAT, and GPx). To support the activation of antioxidant defense and inhibition of apoptosis in our HMC3 cell model, the bioactive phytochemicals within AHE were identified by HPLC analysis. We found that AHE had high levels of carotenoids (α-carotene, β-carotene, and lutein) and flavonoids (quercetin, luteolin, and kaempferol). Our novel findings indicate that AHE can inhibit glutamate-induced neurotoxicity via ER stress and apoptosis signaling pathways by activating cellular antioxidant enzymes in HMC3 cells, suggesting a potential mechanism for neuroprotection. As such, A. lebbeck leaf might potentially represent a promising source and novel alternative approach for preventing neurodegenerative diseases.

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Section: Resultsmentioning

confidence: 99%

Neuroprotective Effects of Albizia lebbeck (L.) Benth. Leaf Extract against Glutamate-Induced Endoplasmic Reticulum Stress and Apoptosis in Human Microglial Cells

et al. 2023

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Section: Resultsmentioning

confidence: 99%

“…With a root mean square deviation (RMSD) value lower than the crystallographic resolution of 6RQ4, these results validated the molecular docking methodology in accordance with previous studies. 27 The MLG-ERK complex displayed RMSD values below 1 (Figure 6A), indicating that MLG binds deeply within the cavity, resulting in a low binding energy of 7.23 kcal/mol through interactions with amino acids such as TYR 36, VAL 39, LYS 54, GLU 71, CYS 166, ASP 167, and LEU 156. The TYR 36 phenol ring exhibited an "out" conformation, consistent with other ERK-specific ATP-competitive inhibitor conformations.…”

Section: Molecular Docking Of Erk To Mlgmentioning

confidence: 99%

Preventive Effect of 1-Methoxylespeflorin G11 on Nitrite Release in Lipopolysaccharide-Stimulated Glial Cells

Paing,

Valencia,

Cho

et al. 2023

Natural Product Communications

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Neuroinflammation is a critical factor in the onset and progression of various brain disorders. Upon exposure to inflammatory stimuli, glial cells become activated, releasing excessive proinflammatory mediators that exacerbate neuropathological conditions. Nitric oxide contributes to neuroinflammation, neurotoxicity, and neuronal death, making its regulation in activated glial cells essential for treating neuroinflammation. Lespedeza bicolor, a traditional medicine used for fever, cough, and nephritis treatment, has a neuroprotective effect attributed to the pterocarpan 1-methoxylespeflorin G11 (MLG), as identified in our previous study. This study examines the protective role of MLG in lipopolysaccharide (LPS)-stimulated glial cells. We found that MLG treatment attenuated LPS-induced nitrite release by downregulating inducible nitric oxide synthase expression in astrocytes. Additionally, MLG impeded LPS-induced nuclear translocation of the p65 subunit of nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-κB) and decreased LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK). The MLG demonstrated similar inhibitory effects on nitrite release and p65 nuclear translocation in microglial cells. Molecular docking analyses unveiled the potential binding mode of MLG to ERK. Collectively, our results indicate that MLG may possess therapeutic potential in treating neuroinflammatory diseases by suppressing nitrite release in glial cells.

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“…These applications include the treatment of ischemia/reperfusion injury, as well as antimicrobial, anticancer, and SARS-CoV PLpro inhibition. Additionally, KEAP1-NRF2 inhibitors containing naphthalene moieties are being explored for their potential in treating COVID-19 [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Design, synthesis, biochemical and in silico characterization of novel naphthalene-thiourea conjugates as potential and selective inhibitors of alkaline phosphatase

et al. 2023

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Naphthalene ring is present in a number of FDA-approved, commercially available medications, including naphyrone, terbinafine, propranolol, naproxen, duloxetine, lasofoxetine, and bedaquiline. By reacting newly obtained 1-naphthoyl isothiocyanate with properly modified anilines, a library of ten novel naphthalene-thiourea conjugates ( 5a–5j ) were produced with good to exceptional yields and high purity. The newly synthesized compounds were observed for their potential to inhibit alkaline phosphatase (ALP) and scavenge free radicals. All of the investigated compounds displayed a more powerful inhibitory profile than the reference agent, KH 2 PO 4 particularly compound 5h and 5a exhibited strong inhibitory potential against ALP with IC 50 value of 0.365 ± 0.011 and 0.436 ± 0.057 µM respectively. In addition, Lineweaver–Burk plots revealed the non-competitive inhibition mode of the most powerful derivative i.e., 5h ( ki value 0.5 µM). To investigate the putative binding mode of selective inhibitor interactions, molecular docking was performed. It is recommended that future research will focus on developing selective alkaline phosphatase inhibitors by modifying the structure of the 5h derivative.

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Neuroprotective effects of phenolic glycosides from Populus tomentiglandulosa roots in HT22 mouse hippocampal neuronal cells

Cited by 3 publications

References 39 publications

Neuroprotective Effects of Albizia lebbeck (L.) Benth. Leaf Extract against Glutamate-Induced Endoplasmic Reticulum Stress and Apoptosis in Human Microglial Cells

Neuroprotective Effects of Albizia lebbeck (L.) Benth. Leaf Extract against Glutamate-Induced Endoplasmic Reticulum Stress and Apoptosis in Human Microglial Cells

Preventive Effect of 1-Methoxylespeflorin G11 on Nitrite Release in Lipopolysaccharide-Stimulated Glial Cells

Design, synthesis, biochemical and in silico characterization of novel naphthalene-thiourea conjugates as potential and selective inhibitors of alkaline phosphatase

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