Flavanonol Taxifolin Attenuates Proteasome Inhibition-Induced Apoptosis in Differentiated PC12 Cells by Suppressing Cell Death Process

Nam, Yoon Jeong; Lee, Da Hee; Shin, Yong Kyoo; Sohn, Dong Suep; Lee, Chung Soo

doi:10.1007/s11064-014-1493-x

Cited by 17 publications

(7 citation statements)

References 49 publications

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“…In this study, similar results were also obtained in hepatic oxidative stress indicators after modeling with LPS. As an effective antioxidant [ 42 ], most of the antioxidant activity of DHQ had been confirmed in vitro or in therapy models [ 43 , 44 ]. Previous reports have indicated that the antioxidant effect of DHQ may act through binding of metal ions [ 43 ] and inhibiting enzymatic reactions [ 45 ], leading to free radical formation as well as inhibiting lipid peroxidation [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of Dihydroquercetin on Energy Metabolism in LPS-Induced Inflammatory Mice

Hussein

et al. 2022

BioMed Research International

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This study investigated the effects and alterations of dihydroquercetin on the growth performance, nutriment metabolism, antioxidant and immune function, and energy substrate utilization in lipopolysaccharide-challenged mice. A total of 0, 50, and 200 mg/kg of dihydroquercetin were intragastrically administered once a day for 21 days. After the pretreatment with dihydroquercetin, each group was subjected to a lipopolysaccharide challenge (except for the control group). After lipopolysaccharide injection, food intake, body weight, metabolic indexes of blood and liver nutrients, blood inflammatory factors, and liver oxidative stress indexes were measured at 6, 12, 24, and 48 h, respectively. Indirect calorimetry analysis was performed by respiratory gas analysis for 48 h to calculate the energy substrate metabolism of carbohydrate, fat, and protein. Urinary nitrogen excretion was measured to evaluate the urinary protein metabolism to calculate the substrate utilization. The results showed that dihydroquercetin pretreatment can significantly increase the weight gain and average food intake and decrease the mortality rate in lipopolysaccharide-induced inflammation mice. Furthermore, dihydroquercetin pretreatment can alleviate the negative effects of lipopolysaccharides by increasing levels of superoxide dismutase and glutathione peroxidase and by decreasing the malondialdehyde and serum inflammatory cytokines (interleukin-1β, nuclear factor κB, and interleukin-6). Dihydroquercetin pretreatment also can relieve nutrient metabolic disorder by increasing blood glucose, serum total protein, and liver glycogen levels and reducing serum and liver triglycerides, serum cholesterol, serum lactate dehydrogenase, and serum urea nitrogen levels. Meanwhile, it increases the relative utilization of carbohydrate, reducing relative utilization of protein and lipid, alleviating the change in energy metabolism pattern from glucose-predominant to lipid-predominant caused by lipopolysaccharide stimulation. In addition, the degree of metabolic pattern transformation depends on the dose of dihydroquercetin supplement. Finally, according to principal component analysis, we found that the inflammation was strongest in the mice at 24 h and was subsequently relieved in the LPS-stimulated group, whereas in the dihydroquercetin-pretreated group, the inflammation was initially relieved. To summarize, dihydroquercetin pretreatment can improve energy metabolism disorder and attenuate the negative effects of lipopolysaccharide challenge in mice from the initial stage of inflammation.

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Section: Discussionmentioning

confidence: 99%

Effect of Dihydroquercetin on Energy Metabolism in LPS-Induced Inflammatory Mice

Hussein

et al. 2022

BioMed Research International

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“…In previous research, taxifolin suppressed the development of oxidative stress in the lung tissue of cisplatin-treated animals. Studies also reported that taxifolin suppressed MDA production in a PC12 cell line [25] and that it provided protection against inflammatory-induced damage in the lung tissue in an experimental study by suppressing MPO activity [26]. No previous studies have investigated the effect of taxifolin on tGSH in the lung tissue or its effect on DNA oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Taxifolin on Cisplatin-Induced Pulmonary Damage in Rats: A Biochemical and Histopathological Evaluation

Ünver

Tosun

Ölmez

et al. 2019

Mediators of Inflammation

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The effect of taxifolin on cisplatin-induced oxidative pulmonary damage was investigated biochemically and histopathologically in male albino Wistar rats. There were four groups, with six animals in each group: 50 mg/kg of taxifolin plus 2.5 mg/kg of cisplatin (TC) group, 2.5 mg/kg of cisplatin only (CIS) group, 50 mg/kg of taxifolin only (TG) group, and a healthy control group (HG). In terms of the experimental procedure, the animals in the TC and TG groups were first treated via oral gavage. The CIS and HG groups received distilled water as solvent, respectively. One hour later, the TC and CIS groups received cisplatin at a dose of 2.5 mg/kg (injected intraperitoneally). Taxifolin, cisplatin, and the distilled water were administered at the indicated dose and volume, using the same method daily for 14 d. At the end of this period, the animals were killed with a high dosage of thiopental anaesthesia (50 mg/kg). Blood and lung tissue samples were taken for biochemical (malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), and 8-hydroxy-2 deoxyguanosine (8-OHdG)) analyses and histopathological examinations. The biochemical and histopathological results in the TC and HG groups were then compared with those in the CIS group. Cisplatin increased the levels of MDA, myeloperoxidase, and 8-OHdG, a marker of oxidative DNA damage, and reduced the amount of tGSH in the lung tissue. Moreover, severe alveolar damage, including oedema and extensive alveolar septal fibrosis, in addition to infiltration of polymorphic nuclear leucocytes and haemorrhagic foci, was observed in the CIS group. These histopathological findings demonstrate that taxifolin provides protection against pulmonary oxidative stress by preventing increases in oxidant parameters and decreases in antioxidants.

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“…Behavior after the test, the rats in all groups randomly selected 30 rats (5) in each group, with 10 % chloral hydrate anesthesia in rats, with 2.5 % glutaraldehyde perfusion fixed phosphate buffer, quickly put to death and brain tissue of rats are extracted, isolated hippocampal tissue, will be isolated from the hippocampus to clean phosphate buffer, ultra-thin slicing machine slices after polymerization, observed by TEM to observe and record the value.…”

Section: Transmission Electron Microscope (Tem) Observationmentioning

confidence: 99%

“…Traditional Chinese Medicine (TCM) believes that the loss of medullary sea and insufficiency of renal essence are the main pathogenesis of senile dementia [4] . It is certain that the pathogenesis of senile dementia is closely related to the generation of SPs [5] . Age spots are not solubility of plaques in the brain organization, its main composition is extracellular beta-amyloid, autopsy study found that patients with AD in AD patients in the body of Amyloid-beta (Aβ) 1-42 may also appear in the normal brain tissue, the protein in brain tissue of precipitation accumulated a large number of local space and converge into age spots, such change is brain tissue to combat AD cause related injury of a kind of brain tissue damage metabolic mechanism [6,7] .…”

mentioning

confidence: 99%

Zuogui Pill on Heat Shock Protein 70 and Ultrastructure of Brain Neurons in Senile Dementia Model Rats

Peng¹,

Liu²,

Tang³

et al. 2022

IJPS

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Peng et al.: Zuogui Pill on Heat Shock Protein 70 and Ultrastructure of Brain Neurons Alzheimer's disease is a pathological mechanism of chronic degenerative disease of brain function, which has a profound influence on various brain diseases, with the highest incidence in the elderly population. With the deepening of population aging, the incidence of Alzheimer's disease is also on the rise, seriously affecting the quality of life of the elderly population. Therefore, the study of neuronal heat shock protein 70 and its ultrastructure is helpful to enhance the therapeutic effect and improve the quality of life of patients. To observe the effect of Zuogui pill on heat shock protein and ultrastructure of brain neurons in rats with Alzheimer's disease. The experimental rats were divided into model group, anti-cerebral failure control group, Haboin control group, Zuogui pill low-dose group, Zuogui pill high-dose group and sham operation group. The model group was injected with D-galactose intraperitoneal injection and amyloid-beta injection into the hippocampus to prepare an Alzheimer's disease animal model. The two control groups were injected with anti-Nao Shuai capsule and Haberman capsule while modeling. The sham operation group was injected with the same amount of normal saline into the hippocampus of both rats. After successful modeling, acetylcholinesterase of rat brain homogenate was detected by biochemical method, expression of heat shock protein 70 in hippocampus of rats in each group was measured by reverse transcription-polymerase chain reaction and ultrastructural changes of rat brain neurons were observed by transmission electron microscope. Zuogui pill could inhibit acetylcholinesterase activity, reduce apoptosis and stabilize the number of neurons. Ultrastructural observation also showed that hippocampal neurons in each treatment group showed morphological characteristics different from the early apoptosis in the model group. Zuogui pill has a positive effect on increasing the number of neurons surviving and inhibiting cell death. It can effectively promote the repair of nerve cells in the brain, thus improving memory impairment in Alzheimer's disease patients.

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Flavanonol Taxifolin Attenuates Proteasome Inhibition-Induced Apoptosis in Differentiated PC12 Cells by Suppressing Cell Death Process

Cited by 17 publications

References 49 publications

Effect of Dihydroquercetin on Energy Metabolism in LPS-Induced Inflammatory Mice

Effect of Dihydroquercetin on Energy Metabolism in LPS-Induced Inflammatory Mice

The Effect of Taxifolin on Cisplatin-Induced Pulmonary Damage in Rats: A Biochemical and Histopathological Evaluation

Zuogui Pill on Heat Shock Protein 70 and Ultrastructure of Brain Neurons in Senile Dementia Model Rats

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