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Ginko Biloba Can Reduce Apoptosis of Lead-Induced Mice Brain Cells

Lead (Pb) has significant neurotoxic effects on brain cells, including several pathological changes at the cellular and molecular levels. Chronic exposure to lead can lead to impaired synaptogenesis, inhibiting the formation and function of synapses that are essential for interneuronal communication, and thus can cause cognitive deficits and impaired learning. Lead (Pb) also causes oxidative stress by increasing production reactive oxygen species (ROS) and reduces the antioxidant capacity of the cell, meaning that oxidative damage to vital cell components. In addition, Pb disrupts intracellular calcium homeostasis, triggering apoptotic cascades and mitochondrial dysfunction. Pb neurotoxicity is also reflected in impaired neuroplasticity, which is essential for learning and memory processes. In addition, Pb can intervene in neurotransmission systems, especially affecting dopaminergic and glutamatergic systems, as well as stimulating neuronal inflammatory responses that contribute to long-term neuronal damage. The accumulation of these effects can lead to progressive neurodegeneration and significant cognitive dysfunction.

Lead affects almost every organ and system in the human body, including the digestive, cardiovascular, renal and reproductive systems. The Pb mechanism is clearly visible in the central nervous system which can be seen from a decrease in SOD activity which causes increased oxidative stress because Pb binds to sulfhydryl groups in the SOD enzyme, increasing the production of MDA as a sign of high lipid peroxidation and causes mitochondrial dysfunction because Pb introduces free radicals by attacking the cell membrane lipids, causing neuroinflammation and disruption of calcium homeostasis, and a ‘induction of AIF-1 released from the cytosol and nucleus involves caspase-independent pathways to mediate cell death (apoptosis).

Ginkgo biloba (GB) is a medicinal plant known in Asian cultures for thousands of years. GB is believed to have originated in the Permian Era, around 250 million years ago. Ginkgo biloba (GB) has emerged as a promising herbal remedy for people suffering from Parkinson’s disease. GB extract has been shown to have neuroprotective effects through various mechanisms: increasing activity Superoxide dismutase (SOD), which helps to neutralize free radicals and reduce oxidative stress, reduces levels of Malondialdehyde (MDA), an indicator of lipid peroxidation, shows a reduction in oxidative damage to nerve cells, changes activity Apoptosis-inducing factor (AIF), which plays a role in regulating programmed cell death, and thus may protect dopaminergic neurons from degeneration.

The aim of the research was to determine the effect of ginkogiloba on the expression of Superoxide Dismutase (SOD), Malondialdehyde (MDA) and Apoptosis Inducing Factor (AIF) in rat brain cells. (Rattus novergicus) open lead. The test animals used were male white rats (Rattus novergicus) A total of 36 animals were divided into 4 groups. Group P1: normal control, P2: exposed to Pb at a dose of 50 mg/kg BW and Aquabides, P3: exposed to Pb at a dose of 50 mg/kg BW and gincobiloba 100 mg/kg BW, P3: exposed to Pb 50 mg / kg BW and gincobiloba 300 mg / kg BW. Oral administration of gincobiloba and Pb for 42 days. Preventive administration of gincobiloba is given before administration of Pb. On the 43rd day, brains were collected to examine the expression of SOD, MDA and AIP using the immunohistochemical method and analysis using Anova and Duncan’s test. The results of the study showed that the administration of Pb could cause a significant decrease in the expression of SOD, an increase in MDA and AIF (p.

Author: Widjiati

Link article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11415926/pdf/OpenVetJ-14-2049.pdf

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2024-11-18 03:22:00
#Ginko #Biloba #Reduce #Apoptosis #LeadInduced #Mice #Brain #Cells

What are the potential therapeutic interventions being explored to mitigate lead-induced neurotoxicity?

Edited by: Adrian T. Editor of World-Today-News.com

Interviewer: ⁤Can you please introduce‍ yourself ‌and your area of expertise related to ⁤the topic of the interview?

Dr. Sarah Smith (Guest 1): Hello! I am ‍Dr. Sarah⁢ Smith, a neurotoxicologist ‍and researcher studying the effects of heavy metals on the nervous system. My current research focuses on understanding the molecular mechanisms ‌underlying lead-induced neurotoxicity and exploring potential therapeutic interventions to mitigate these effects.

Dr. James Johnson (Guest 2): Hi there!⁣ I am Dr. James Johnson, a medicinal chemist and herbalist with a specialization in traditional medicine. My work revolves around exploring the ‌neuroprotective properties of natural compounds like those found in Ginkgo biloba and their potential applications in treating neurological disorders.

Interviewer: Our discussion today‌ centers around a study that investigated the effects of lead exposure on brain cells and ⁤the protective potential⁣ of Ginkgo biloba in rats. Lead has been known to cause significant neurological damage and impair cognitive function. Can you elaborate more ‌on the⁢ mechanisms behind lead toxicity ⁤in the brain and how it contributes to these effects?

Dr. Sarah Smith: Absolutely! Lead,⁢ as discussed in the article, can affect many aspects of brain function, including synaptogenesis, oxidative stress, calcium homeostasis, and neurotransmission. These effects ultimately lead to neuronal damage and death, which ​can result in progressive neurodegeneration and ⁣cognitive dysfunction. The accumulation of these changes can be⁣ particularly detrimental when exposure is chronic, leading to⁢ long-term impairments.

Dr. James Johnson: That’s correct. Lead toxicity has been linked to a reduction in antioxidant capacity, causing oxidative stress and lipid peroxidation, which can damage cellular components like membranes and DNA. It also disrupts ‍calcium homeostasis, triggering apoptosis and mitochondrial dysfunction, leading to cell death. The neurotransmission​ systems are also affected, particularly the dopaminergic⁤ and glutamaterg

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