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• Research Paper Volume 13, Issue 21 pp 23913-23935

  New tale on LianHuaQingWen: IL6R/IL6/IL6ST complex is a potential target for COVID-19 treatment

  Relevance score: 5.8979073

  Zhao Tianyu, Cui Xiaoli, Wang Yaru, Zhang Min, Yue Fengli, He Kan, Chen Li, Li Jing

  Keywords: LianHuaQingWen (LHQW), COVID-19, IL6R/IL6/IL6ST complex, quercetin, AGE-RAGE signaling pathway

  Published in Aging on November 3, 2021

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  LianHuaQingWen (LHQW) improves clinical symptoms and alleviates the severity of COVID-19, but the mechanism is unclear. This study aimed to investigate the potential molecular targets and mechanisms of LHQW in treating COVID-19 using a network pharmacology-based approach and molecular docking analysis. The main active ingredients, therapeutic targets of LHQW, and the pathogenic targets of COVID-19 were screened using the TCMSP, UniProt, STRING, and GeneCards databases. According to the “Drug-Ingredients-Targets-Disease” network, Interleukin 6 (IL6) was identified as the core target, and quercetin, luteolin, and wogonin as the active ingredients of LHQW associated with IL6. The response to lipopolysaccharide was the most significant biological process identified by gene ontology enrichment analysis, and AGE-RAGE signaling pathway activation was prominent based on the interaction between LHQW and COVID-19. Protein-protein docking analysis showed that IL6 receptor (IL6R)/IL6/IL6 receptor subunit beta (IL6ST) and Spike protein were mainly bound via conventional hydrogen bonds. Furthermore, protein-small molecule docking showed that all three active ingredients could bind stably in the binding model of IL6R/IL6 and IL6ST. Our findings suggest that LHQW may inhibit the lipopolysaccharide-mediated inflammatory response and regulate the AGE-RAGE signaling pathway through IL6. In addition, the N-terminal domain of the S protein of COVID-19 has a good binding activity to IL6ST, and quercetin and wogonin in LHQW may affect IL6ST-mediated IL6 signal transduction and a large number of signaling pathways downstream to other cytokines by directly affecting protein-protein interaction. These findings suggest the potential molecular mechanism by which LHQW inhibits COVID-19 through the regulation of IL6R/IL6/IL6ST.

• Research Paper Volume 13, Issue 8 pp 11738-11751

  Administration of quercetin improves mitochondria quality control and protects the neurons in 6-OHDA-lesioned Parkinson's disease models

  Relevance score: 6.4770675

  Wen-Wen Wang, Ruiyu Han, Hai-Jun He, Jia Li, Si-Yan Chen, Yingying Gu, Chenglong Xie

  Keywords: quercetin, Parkinson's disease, mitophagy, mitochondria quality control

  Published in Aging on April 20, 2021

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  Mounting evidence suggests that mitochondrial dysfunction and impaired mitophagy lead to Parkinson’s disease (PD). Quercetin, one of the most abundant polyphenolic flavonoids, displays many health-promoting biological effects in many diseases. We explored the neuroprotective effect of quercetin in vivo in the 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD and in vitro in 6-OHDA-treated PC12 cells. In vitro, we found that quercetin (20 μM) treatment improved mitochondrial quality control, reduced oxidative stress, increased the levels of the mitophagy markers PINK1 and Parkin and decreased α-synuclein protein expression in 6-OHDA-treated PC12 cells. Moreover, our in vivo findings demonstrated that administration of quercetin also relieved 6-OHDA-induced progressive PD-like motor behaviors, mitigated neuronal death and reduced mitochondrial damage and α-synuclein accumulation in PD rats. Furthermore, the neuroprotective effect of quercetin was suppressed by knockdown of either Pink1 or Parkin.

• Research Paper Volume 12, Issue 8 pp 7015-7029

  Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice

  Relevance score: 8.079396

  Tian Hu, Jing-Jing Shi, Jiansong Fang, Qi Wang, Yun-Bo Chen, Shi-Jie Zhang

  Keywords: quercetin, diabetic encephalopathy, SIRT1, ER stress

  Published in Aging on April 20, 2020

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  Studies have shown that diabetes is an important risk factor for cognitive dysfunction, also called diabetic encephalopathy (DE). Quercetin has been reported to be effective in improving cognitive dysfunction in DE. But its detailed mechanism is still ambiguous. In this study, we used db/db mice to investigate whether quercetin could activate SIRT1 and inhibit ER pathways to improve DE. Behavioral tests (Morris water maze and new objects) showed that quercetin (70 mg/kg) can effectively improve the learning and memory ability in db/db mice. OGTT and ITT tests indicated that quercetin could alleviate impaired glucose tolerance and insulin resistance in db/db mice. Western blot analysis and Nissl staining showed that quercetin can improve the expression of nerve and synapse-associated proteins (PSD93, PSD95, NGF and BDNF) and inhibit neurodegeneration. Meanwhile, quercetin up-regulates SIRT1 protein expression and inhibits the expression of ER signaling pathway-related proteins (PERK, IRE-1α, ATF6, eIF2α, BIP and PDI). In addition, oxidative stress levels were significantly reduced after quercetin treatment. In conclusion, current experimental results indicated that SIRT1/ER stress is a promising mechanism involved in quercetin-treated diabetic encephalopathy.

  

  Quercetin improves learning and memory impairment in db/db mice. (A) The chemical structure of Quercetin. (B) Escape latency of the five day in MWM. (C) Swimming paths of the db/db mice on the first and fifth day in MWM. (D) Time spent in the target quadrant in in MWM. (E) Crossing times of the target platform in MWM. (F) Novel object preference index in NOR. Quercetin-L: 35mg/kg/d; Quercetin-H: 70mg/kg/d. Data represent mean ± SEM (n = 10 per group). #p < 0.05, ##p < 0.01, ###p < 0.001vs. db/m; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/db.

  
  
  

  

  Quercetin alleviates impaired glucose tolerance and insulin resistance in db/db mice. (A) Body Weight. (B) OGTT. (C) OGTT-AUC. (D) ITT. (E) ITT-AUC. Quercetin-L: 35mg/kg/d; Quercetin-H: 70mg/kg/d. Data represent mean ± SEM (n = 10 per group). #p < 0.05, ##p < 0.01, ###p < 0.001vs. db/m; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/db.

  
  
  

  

  Quercetin decreases oxidative stress in db/db mice. (A) MDA. (B) SOD. (C) CAT. (D) GSH-PX. Quercetin-L: 35mg/kg/d; Quercetin-H: 70mg/kg/d. Data represent mean ± SEM (n = 10 per group). #p < 0.05, ##p < 0.01, ###p < 0.001vs. db/m; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/db.

  
  
  

  

  Quercetin protects against neuronal apoptosis in the brain of db/db mice. Western blot analysis: (A) Caspase3; (B) Bax/Bcl2. Quercetin-L: 35mg/kg/d; Quercetin-H: 70mg/kg/d. Data represent mean ± SEM (n = 10 per group). #p < 0.05, ##p < 0.01, ###p < 0.001vs. db/m; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/db.

  
  
  

  

  Quercetin increases neurotrophic factor levels in the brain of db/db mice. Western blot analysis: (A) PSD93; (B) PSD95; (C) NGF; (D) BDNF. Quercetin-L: 35mg/kg/d; Quercetin-H: 70mg/kg/d. Data represent mean ± SEM (n = 10 per group). #p < 0.05, ##p < 0.01, ###p < 0.001vs. db/m; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/db.

  
  
  

  

  Quercetin ameliorates neurodegeneration in db/db mice. (A) Nissl’s staining. (B) Immunofluorescence of NGF. Scale bar: 100 μm.

  
  
  

  

  Quercetin activates SIRT1 in the brain of db/db mice. (A) Immunofluorescence of SIRT1 in hippocampus. (B) Immunofluorescence of sirt1 in cortex. Scale bar: 100 μm.

  
  
  

  

  Quercetin activates SIRT1 and relieves ER stress in db/db mice. Western blot analysis: (A) SIRT1; (B) P-PERK/PERK; (C) P-IRE1α/IRE1α; (D) ATF6; (E) BIP; (F) PDI; (G) P-eIF2α/eIF2α. Quercetin-L: 35mg/kg/d; Quercetin-H: 70mg/kg/d. Data represent mean ± SEM (n = 10 per group). #p < 0.05, ##p < 0.01, ###p < 0.001vs. db/m; * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/db.

  
  
  

• Research Perspective Volume 12, Issue 8 pp 6511-6517

  COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?

  Relevance score: 4.207054

  Camillo Sargiacomo, Federica Sotgia, Michael P. Lisanti

  Keywords: COVID-19, corona virus, aging, senescence, senolytic drug therapy, prevention, viral replication, drug repurposing, antibiotic, Azithromycin, Hydroxy-chloroquine, Rapamycin, Doxycycline, Quercetin

  Published in Aging on March 30, 2020

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  COVID-19, also known as SARS-CoV-2, is a new emerging zoonotic corona virus of the SARS (Severe Acute Respiratory Syndrome) and the MERS (Middle East Respiratory Syndrome) family. COVID-19 originated in China and spread world-wide, resulting in the pandemic of 2020. For some reason, COVID-19 shows a considerably higher mortality rate in patients with advanced chronological age. This begs the question as to whether there is a functional association between COVID-19 infection and the process of chronological aging. Two host receptors have been proposed for COVID-19. One is CD26 and the other is ACE-2 (angiotensin-converting enzyme 2). Interestingly, both CD26 and the angiotensin system show associations with senescence. Similarly, two proposed therapeutics for the treatment of COVID-19 infection are Azithromycin and Quercetin, both drugs with significant senolytic activity. Also, Chloroquine-related compounds inhibit the induction of the well-known senescence marker, Beta-galactosidase. Other anti-aging drugs should also be considered, such as Rapamycin and Doxycycline, as they behave as inhibitors of protein synthesis, blocking both SASP and viral replication. Therefore, we wish to speculate that the fight against COVID-19 disease should involve testing the hypothesis that senolytics and other anti-aging drugs may have a prominent role in preventing the transmission of the virus, as well as aid in its treatment. Thus, we propose that new clinical trials may be warranted, as several senolytic and anti-aging therapeutics are existing FDA-approved drugs, with excellent safety profiles, and would be readily available for drug repurposing efforts. As Azithromycin and Doxycycline are both commonly used antibiotics that inhibit viral replication and IL-6 production, we may want to consider this general class of antibiotics that functionally inhibits cellular protein synthesis as a side-effect, for the treatment and prevention of COVID-19 disease.

  

  What is the relationship between COVID-19 and advanced chronological age? Here, we suggest that the COVID-19 corona virus preferentially targets senescent lung cells, resulting in increased morbidity and mortality in the aging population. One possible solution for prevention/treatment would be the use of senolytics or other anti-aging drugs. Testing this hypothesis will require the necessary clinical trials, with a focus on drug repurposing.