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RISS 인기검색어
- 검색키워드
- 저자 : Murad Ali Shah (검색결과 27 건)
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Murad-Ali Shah,Ju-Bin Kang,Myeong Ok Kim,Phil-Ok Koh 대한수의학회 2022 Journal of Veterinary Science Vol.23 No.6
Background: Stroke is caused by disruption of blood supply and results in permanent disabilities as well as death. Chlorogenic acid is a phenolic compound found in various fruits and coffee and exerts antioxidant, anti-inflammatory, and anti-apoptotic effects. Objectives: The purpose of this study was to investigate whether chlorogenic acid regulates the PI3K-Akt-Bad signaling pathway in middle cerebral artery occlusion (MCAO)-induced damage. Methods: Chlorogenic acid (30 mg/kg) or vehicle was administered peritoneally to adult male rats 2 h after MCAO surgery, and animals were sacrificed 24 h after MCAO surgery. Neurobehavioral tests were performed, and brain tissues were isolated. The cerebral cortex was collected for Western blot and immunoprecipitation analyses. Results: MCAO damage caused severe neurobehavioral disorders and chlorogenic acid improved the neurological disorders. Chlorogenic acid alleviated the MCAO-induced histopathological changes and decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. Furthermore, MCAO-induced damage reduced the expression of phospho-PDK1, phospho-Akt, and phospho-Bad, which was alleviated with administration of chlorogenic acid. The interaction between phospho-Bad and 14-3-3 levels was reduced in MCAO animals, which was attenuated by chlorogenic acid treatment. In addition, chlorogenic acid alleviated the increase of cytochrome c and caspase-3 expression caused by MCAO damage. Conclusions: The results of the present study showed that chlorogenic acid activates phospho-Akt and phospho-Bad and promotes the interaction between phospho-Bad and 14-3-3 during MCAO damage. In conclusion, chlorogenic acid exerts neuroprotective effects by activating the Akt-Bad signaling pathway and maintaining the interaction between phospho-Bad and 14-3-3 in ischemic stroke model.
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Murad Ali Shah,강주빈,고필옥 한국실험동물학회 2023 Laboratory Animal Research Vol.39 No.2
Background: Cerebral ischemia is a serious neurological disorder that can lead to high morbidity and mortality. Chlorogenic acid is a polyphenol compound with antioxidant that can regulate proteins in cerebral ischemia. Middle cerebral artery occlusion (MCAO) surgery was performed to induce ischemic brain injury and was maintained for 24 h. Chlorogenic acid (30 mg/kg) or vehicle was administrated into the peritoneal cavity 2 h after MCAO surgery. The cerebral cortical tissues were collected for further study and a proteomic approach was performed to identify the proteins changed by chlorogenic acid in the MCAO animals. Results: We found that chlorogenic acid alleviated in changes in adenosylhomocysteinase, glycerol-3-phosphate dehydrogenase, eukaryotic translation initiation factor 4A-II, apolipoprotein A-I, and mu-crystallin. These proteins were reduced in MCAO animals with vehicle, and these reductions were attenuated by chlorogenic acid treatment. The mitigation of this reduction by chlorogenic acid was confirmed by the reverse transcription PCR technique. These proteins are associated with energy metabolism, protein synthesis, inflammation, and physiological metabolism. They are involved in the neuroprotective effect of chlorogenic acid. These results showed that chlorogenic acid alleviates the neurological disorders caused by MCAO and regulates the expression of proteins involved in neuroprotection. Conclusions: Therefore, our findings provide evidence that chlorogenic acid plays a neuroprotective role in stroke animal models by controlling specific proteins.
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Murad-Ali Shah,박동주,강주빈,김명옥,고필옥 한국실험동물학회 2020 Laboratory Animal Research Vol.36 No.3
Baicalin is a natural flavonoid that exerts a variety of pharmaceutical effects such as anti-inflammatory and antioxidant. Lipopolysaccharide (LPS) is an endotoxin that releases inflammatory cytokines and induces inflammatory response. This study was investigated the anti-inflammatory mechanism of baicalin against LPS-induced inflammatory response in the hippocampus. Adult mice were randomly grouped into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250 μg/kg/day) and baicalin (10 mg/kg/day) were administered intraperitoneally for 7 consecutive days. We measured neuroglia cells activation and inflammatory factors activation using Western blot analysis and immunofluorescence staining techniques. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are widely used as microglia and astrocyte markers, respectively. LPS treatment increased Iba-1 and GFAP expression, while baicalin co-treatment attenuated this overexpression. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammation. Baicalin co-treatment alleviated LPS-induced increase of NF-κB in the hippocampus. In addition, LPS treatment upregulated pro-inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). However, baicalin co-treatment prevented LPS-induced increases of IL-1β and TNF-α in the hippocampus. Results from the present study showed that baicalin suppresses LPS-induced neuroinflammation by regulating microglia and astrocyte activation and modulating inflammatory factors in the hippocampus. Thus, these results demonstrate that baicalin has neuroprotective effect by alleviates microglia and astrocyte activation and modulates inflammatory response by suppressing NF-κB expression in hippocampus with neuroinflammation caused by LPS.
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Murad-Ali Shah, Yeung Bae Jin, Myeong-Ok Kim, Phil-Ok Koh 한국예방수의학회 2023 예방수의학회지 Vol.47 No.3
Ischemic stroke causes severe neuronal damage. Chlorogenic acid is a phenolic substance present in fruits and coffee. It also exerts neuroprotective effects against various brain injuries. The 14-3-3 family protein perform a variety of functions including metabolism, signal transduction, cell differentiation, and apoptosis. The purpose of this study is to investigate whether chlorogenic acid regulates the expression of 14-3-3 protein in stroke animal models. Ischemic stroke was induced by middle cerebral artery occlusion (MCAO) surgery. Phosphate buffered saline (PBS) or chlorogenic acid (30 mg/kg) were intraperitoneally injected to adult male rats 2 h before MCAO surgery. Adhesive-removal test was performed 24 h after MCAO surgery and cerebral cortical tissues were collected for further study. MCAO damage caused severe neurological impairment and chlorogenic acid treatment ameliorated this disorder. Our proteomic approach showed a decrease in 14-3-3 expression in MCAO animals with PBS. The decrease in 14-3-3 expression alleviated in MCAO animal with chlorogenic acid. We confirmed changes in various 14-3-3 protein isoforms, including beta/alpha, zeta/delta, gamma, epsilon, eta, and tau through reverse transcription-PCR. These results explained that chlorogenic acid regulates the expression of 14-3-3 protein in MCAO-induced cerebral ischemia. 14-3-3 is considered to be an important protein for cell survival through binding to pro-apoptotic proteins. The maintenance of 14-3-3 levels is an important event in neuroprotection against ischemic injury. Therefore, we can demonstrate that the 14-3-3 protein contributes to the neuroprotective effect of chlorogenic acid in stroke animal models.
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Murad-Ali Shah,강주빈,박동주,고필옥 한국실험동물학회 2023 Laboratory Animal Research Vol.39 No.1
Background : Epigallocatechin gallate (EGCG) is a flavonoid compound commonly found in green tea. It exhibits antioxidant, anti-inflammatory, and neuroprotective effects in cerebral ischemia. Protein phosphatase 2 A (PP2A) is an important serine/threonine phosphatase enzyme involved in various cellular activities. PP2A subunit B is present abundantly in the brain and plays an important role in the nervous system. We investigated the effect of EGCG on the expression level of PP2A subunit B in cerebral ischemia caused by middle cerebral artery occlusion (MCAO). EGCG (50 mg/kg) or vehicle was injected into the peritoneal cavity prior to MCAO surgery. Neurological behavior tests were performed 24 h after MCAO, and right cerebral cortex tissue was collected. Cerebral ischemia caused serious neurological abnormalities, which were alleviated by EGCG administration. We screened the expression of PP2A subunits containing A, B, and C using reverse-transcription PCR. We confirmed that PP2A subunit B exhibited significant changes in MCAO animals compared to subunits A and C. We continuously examined the expression of PP2A subunit B protein in MCAO animals using Western blot analysis. Results : EGCG alleviated the reduction of PP2A subunit B protein by MCAO damage. In addition, immunohistochemistry demonstrated a decrease in the number of PP2A subunit B-positive cells in the cerebral cortex, and EGCG attenuated this decrease. Maintenance of PP2A subunit B is important for normal brain function. Conclusions : Therefore, our findings suggest that EGCG exerts neuroprotective effects against cerebral ischemia through modulation of PP2A subunit B expression.
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Murad-Ali Shah,Ju-Bin Kang,Dong-Ju Park,Phil-Ok Koh 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Stroke is the global cause of death and permanent disability. Chlorogenic acid has antioxidant, and anti-apoptotic properties. In the current study, we investigated antioxidant and anti-apoptotic properties of chlorogenic acid against middle cerebral artery occlusion (MCAO)-induced cerebral ischemia in adult rats. Rats were injected intraperitoneally with chlorogenic acid (30 mg/kg) or vehicle 2 h after ischemia. After 24 h, cerebral cortex tissues were separated and reactive oxygen species (ROS) and malondialdehyde (MDA) assay, and histopathological analysis were performed. Two-dimensional gel electrophoresis and mass spectrometry techniques were performed to identify protein changes by chlorogenic acid. Results showed a significant increase in both ROS and MDA levels, histopathological lesions, and a high increase in terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the ischemic cerebral cortex. Conversely, chlorogenic acid-treatment significantly reduced these changes in MCAO-induced rats. Moreover, two-dimensional gel electrophoresis and western blot analysis showed significant changes by MCAO surgery. Expression levels of parvalbumin, isocitrate dehydrogenase 1, peroxiredoxin-2, and protein phosphatase 2A subunit A were decreased in the MCAO-induced cortex. However, these decreases were alleviated by chlorogenic acid-treatment. These proteins plays important role in calcium regulation, signal transduction pathways, metabolism, and oxidative stress. These results suggest that chlorogenic acid has neuroprotective properties by regulating of parvalbumin, isocitrate dehydrogenase 1, peroxiredoxin-2, and protein phosphatase 2A subunit A against cerebral ischemic damage. These results further suggest that chlorogenic acid can be used as a neuroprotective agent against diseases related to stroke by regulating various protein expressions. This research was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (NRF-2018R1D1A1B07044074).
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