Phytochemical Analysis and In Vitro and In Vivo Pharmacological Evaluation of Parthenium hysterophorus Linn

Gul, Somia; Khan, Imtiaz; Alnasser, Sulaiman Mohammad; Shah, Syed Muhammad Hassan; Rahman, Md. Mominur

doi:10.1155/2022/6088585

Cited by 3 publications

(1 citation statement)

References 26 publications

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“…5 Ototoxicity refers to the damage caused by drugs that affect the structure of the inner ear and related neural tissues, resulting in cochlear or vestibular dysfunction. [6][7][8][9][10][11] DDP-induced human ototoxicity was more dominant in the cochlea than in the vestibular apparatus. 12 The mechanism of DDP-induced cochlear dysfunction has been associated with cell damage and the destruction of cochlear homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Copper Chaperone Atox1 Protected the Cochlea From Cisplatin by Regulating the Copper Transport Family and Cell Cycle

Chen,

Xiang,

et al. 2023

Int J Toxicol

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Antioxidant 1 copper chaperone (Atox1) may contribute to preventing DDP cochlear damage by regulating copper transport family and cell cycle proteins. A rat model of cochlear damage was developed by placing gelatin sponges treated with DDP in the cochlea. HEI-OC1 cells were treated with 133 μM DDP as a cell model. DDP-induced ototoxicity in rats was confirmed by immunofluorescence (IF) imaging. The damage of DDP to HEI-OC1 cells was assessed by using CCK-8, TUNEL, and flow cytometry. The relationship between Atox1, a member of the copper transport protein family, and the damage to in vivo/ vitro models was explored by qRT-PCR, western blot, CCK-8, TUNEL, and flow cytometry. DDP had toxic and other side effects causing cochlear damage and promoted HEI-OC1 cell apoptosis and cell cycle arrest. The over-expression of Atox1 (oe-Atox1) was accomplished by transfecting lentiviral vectors into in vitro/ vivo models. We found that oe-Atox1 increased the levels of Atox1, copper transporter 1 (CTR1), and SOD3 in HEI-OC1 cells and decreased the expression levels of ATPase copper transporting α (ATP7A) and ATPase copper transporting β (ATP7B). In addition, the transfection of oe-Atox1 decreased cell apoptosis rate and the number of G2/M stage cells. Similarly, the expression of myosin VI and phalloidin of cochlea cells in vivo decreased. Atox1 ameliorated DDP-induced damage to HEI-OC1 cells or rats' cochlea by regulating the levels of members of the copper transport family.

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Section: Introductionmentioning

confidence: 99%

Copper Chaperone Atox1 Protected the Cochlea From Cisplatin by Regulating the Copper Transport Family and Cell Cycle

Chen,

Xiang,

et al. 2023

Int J Toxicol

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Green synthesized silver nanoparticles mediated regulation on hydrolytic enzymes and ROS homeostasis promote growth of three pulses (Cicer arietinum L., Pisum sativum L., and Vigna radiata L.)

Koley,

Mondal,

Mondal

2023

Energ. Ecol. Environ.

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Perspectives on the Molecular Mediators of Oxidative Stress and Antioxidant Strategies in the Context of Neuroprotection and Neurolongevity: An Extensive Review

Shohag

Akhter

Islam

et al. 2022

Oxidative Medicine and Cellular Longevity

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Molecules with at least one unpaired electron in their outermost shell are known as free radicals. Free radical molecules are produced either within our bodies or by external sources such as ozone, cigarette smoking, X-rays, industrial chemicals, and air pollution. Disruption of normal cellular homeostasis by redox signaling may result in cardiovascular, neurodegenerative diseases and cancer. Although ROS (reactive oxygen species) are formed in the GI tract, little is known about how they contribute to pathophysiology and disease etiology. When reactive oxygen species and antioxidants are in imbalance in our bodies, they can cause cell structure damage, neurodegenerative diseases, diabetes, hypercholesterolemia, atherosclerosis, cancer, cardiovascular diseases, metabolic disorders, and other obesity-related disorders, as well as protein misfolding, mitochondrial dysfunction, glial cell activation, and subsequent cellular apoptosis. Neuron cells are gradually destroyed in neurodegenerative diseases. The production of inappropriately aggregated proteins is strongly linked to oxidative stress. This review’s goal is to provide as much information as possible about the numerous neurodegenerative illnesses linked to oxidative stress. The possibilities of multimodal and neuroprotective therapy in human illness, using already accessible medications and demonstrating neuroprotective promise in animal models, are highlighted. Neuroprotection and neurolongevity may improve from the use of bioactive substances from medicinal herbs like Allium stadium, Celastrus paniculatus, and Centella asiatica. Many neuroprotective drugs’ possible role has been addressed. Preventing neuroinflammation has been demonstrated in several animal models.

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Phytochemical Analysis and In Vitro and In Vivo Pharmacological Evaluation of Parthenium hysterophorus Linn

Cited by 3 publications

References 26 publications

Copper Chaperone Atox1 Protected the Cochlea From Cisplatin by Regulating the Copper Transport Family and Cell Cycle

Copper Chaperone Atox1 Protected the Cochlea From Cisplatin by Regulating the Copper Transport Family and Cell Cycle

Green synthesized silver nanoparticles mediated regulation on hydrolytic enzymes and ROS homeostasis promote growth of three pulses (Cicer arietinum L., Pisum sativum L., and Vigna radiata L.)

Perspectives on the Molecular Mediators of Oxidative Stress and Antioxidant Strategies in the Context of Neuroprotection and Neurolongevity: An Extensive Review

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