Ginsenoside Rb1 protects from Staphylococcus aureus-induced oxidative damage and apoptosis through endoplasmic reticulum-stress and death receptor-mediated pathways

Shaukat, Aftab; Shaukat, Irfan; Rajput, Shahid Ali; Shukat, Rizwan; Hanif, Sana; Jiang, Kangfeng; Zhang, Tao; Akhtar, Muhammad Faheem; Shaukat, Imran; Ma, Xiaofei; Liu, Junfeng; Shaukat, Shadab; Umar, Talha; Akhtar, Masood; Yang, Liguo; Deng, Ganzhen

doi:10.1016/j.ecoenv.2021.112353

Cited by 22 publications

(16 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a cell free system, ginsenoside Rb1 can significantly and selectively scavenge hydroxyl radical and hypochlorous acid, two of the strongest reactive oxygen species (ROS), and protect biomacromolecules from oxidative damage ( Lu et al, 2012 ). Ginsenoside Rb1 could inhibit mitochondria-, endoplasmic reticulum stress- and death receptor-mediated apoptotic pathways ( Ke et al, 2021 ; Shaukat et al, 2021 ). Our previous study demonstrated that ginsenoside Rb1 inhibited oxidative stress-induced endoplasmic reticulum stress in rat PC12 cells ( Zeng et al, 2015 ).…”

Section: Pharmacological Effects Of Ginsenoside Rb1mentioning

confidence: 99%

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases

et al. 2022

View full text Add to dashboard Cite

Panax ginseng and Panax notoginseng, two well-known herbs with enormous medical value in Asian countries, have a long usage history in China for the therapy of some diseases, such as stroke. Ginsenoside Rb1 is one of most important active ingredients in Panax ginseng and Panax notoginseng. In the last two decades, more attention has focused on ginsenoside Rb1 as an antioxidative, anti-apoptotic and anti-inflammatory agent that can protect the nervous system. In the review, we summarize the neuroprotective roles of ginsenoside Rb1 and its potential mechanisms in central nervous system diseases (CNSDs), including neurodegenerative diseases, cerebral ischemia injury, depression and spinal cord injury. In conclusion, ginsenoside Rb1 has a potential neuroprotection due to its inhibition of oxidative stress, apoptosis, neuroinflammation and autophagy in CNSDs and may be a promising candidate agent for clinical therapy of CNSDs in the future.

show abstract

Section: Pharmacological Effects Of Ginsenoside Rb1mentioning

confidence: 99%

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Previous studies indicated that MC apoptosis was one of the fundamental pathogenic factors of MIRI, and the inhibition of MC apoptosis was effective in alleviating MIRI ( Zhou et al, 2018 ; Xu et al, 2019 ; Fu D. et al, 2021 ). Ginsenosides can improve MIRI by relieving mitochondria damage, resisting oxidation, reducing inflammatory response, and inhibiting the generation of DISC ( Wang and Roh, 2020 ; Shaukat et al, 2021 ). Ginsenosides can relieve MIRI via multiple signaling pathways, such as the death receptor signaling pathway, mitochondria signaling pathway, PI3K/Akt signaling pathway, NF-κB signaling pathway, and MAPK signaling pathway.…”

Section: Conclusion and Perspectivementioning

confidence: 99%

Inhibition of Myocardial Cell Apoptosis Is Important Mechanism for Ginsenoside in the Limitation of Myocardial Ischemia/Reperfusion Injury

Chen

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Ischemic heart disease has a high mortality, and the recommended therapy is reperfusion. Nevertheless, the restoration of blood flow to ischemic tissue leads to further damage, namely, myocardial ischemia/reperfusion injury (MIRI). Apoptosis is an essential pathogenic factor in MIRI, and ginsenosides are effective in inhibiting apoptosis and alleviating MIRI. Here, we reviewed published studies on the anti-apoptotic effects of ginsenosides and their mechanisms of action in improving MIRI. Each ginsenoside can regulate multiple pathways to protect the myocardium. Overall, the involved apoptotic pathways include the death receptor signaling pathway, mitochondria signaling pathway, PI3K/Akt signaling pathway, NF-κB signaling pathway, and MAPK signaling pathway. Ginsenosides, with diverse chemical structures, regulate different apoptotic pathways to relieve MIRI. Summarizing the effects and mechanisms of ginsenosides contributes to further mechanism research studies and structure–function relationship research studies, which can help the development of new drugs. Therefore, we expect that this review will highlight the importance of ginsenosides in improving MIRI via anti-apoptosis and provide references and suggestions for further research in this field.

show abstract

“…Interestingly, other genes, such as RB1 and CHAMP1 , are also related to oxidative-stress-related processes. It has been suggested that disturbances in RB1 gene expression are involved in DNA damage sensor activity, forkhead box O (Foxo) transcription factors, and p38 mitogen-activated protein kinase processes, for which a disturbed expression affects cell-cycle progression, antioxidant capacity, mitochondrial mass, and cellular metabolism [ 70 , 71 , 72 , 73 , 74 ]. CHAMP1 encodes a protein with a function in kinetochore–microtubule attachment and in the regulation of chromosome segregation.…”

Section: Genetic Basis Of the T13 And T18 Pathogenesesmentioning

confidence: 99%

Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation

Buczyńska

Sidorkiewicz

Hameed

et al. 2022

JCM

View full text Add to dashboard Cite

Autosomal aneuploidies are the most frequently occurring congenital abnormalities and are related to many metabolic disorders, hormonal dysfunctions, neurotransmitter abnormalities, and intellectual disabilities. Trisomies are generated by an error of chromosomal segregation during cell division. Accumulating evidence has shown that deregulated gene expression resulting from the triplication of chromosomes 13 and 18 is associated with many disturbed cellular processes. Moreover, a disturbed oxidative stress status may be implicated in the occurrence of fetal malformations. Therefore, a literature review was undertaken to provide novel insights into the evaluation of trisomy 13 (T13) and 18 (T18) pathogeneses, with a particular concern on the oxidative stress. Corresponding to the limited literature data focused on factors leading to T13 and T18 phenotype occurrence, the importance of oxidative stress evaluation in T13 and T18 could enable the determination of subsequent disturbed metabolic pathways, highlighting the related role of mitochondrial dysfunction or epigenetics. This review illustrates up-to-date T13 and T18 research and discusses the strengths, limitations, and possible directions for future studies. The progressive unification of trisomy-related research protocols might provide potential medical targets in the future along with the implementation of the foundation of modern prenatal medicine.

show abstract

Ginsenoside Rb1 protects from Staphylococcus aureus-induced oxidative damage and apoptosis through endoplasmic reticulum-stress and death receptor-mediated pathways

Cited by 22 publications

References 63 publications

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases

Inhibition of Myocardial Cell Apoptosis Is Important Mechanism for Ginsenoside in the Limitation of Myocardial Ischemia/Reperfusion Injury

Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation

Contact Info

Product

Resources

About