Natural product and Apoptosis Medical Presentation

Natural product and Apoptosis PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Download Free Natural product and Apoptosis medical powerpoint (ppt) presentation for your medical ppt presentation

Tags : medicpresents

Published on : Nov 22, 2017 | Views : 1519 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Natural products and apoptosis Asmaa Ebrahim
Slide 2-

contents Introduction of natural products. Importance of natural products. Ex. Of some natural products with cytotoxic effect on cancer cell lines. vernodalin BTA (Betulonic acid) and OEA (3-oxours-12-en- 28-oic acid).
Slide 3-

Natural product Products from various natural sources. That can be : Extract of entire organism (plant, microorganism). Extract of a part of organism (leaf ,flower of a plant, an isolated gland or other organ of an animal). secondary metabolites with very complex structures, so they are novel structures but, can’t be synthesized and have to be extracted.
Slide 4-

importance Source for some drugs that can’t be synthesized commercially. Supply basic compound that can be modified slightly to be more effective or less toxic. consider as prototypes or models for synthetic drugs that have the same physiologic activities as original (salicylic acid in aspirin). Some compounds have little or no activity, but when modified by chemical or biological method, produce potent drugs (taxol ).
Slide 5-

Centratherum anthelminticum (L.) seeds Kingdom: Plantae Order: Asterales Family: Asteraceae Genus: Centratherum Species : C. anthelminticum Native in India and China. Extract : vernodalin
Slide 6-

Cytotoxic effect of vernodalin against breast tumor cells (MCF-7) CACF-treated cells showed morphological hallmarks of apoptosis including cell shrinkage, lost of cytoskeletal actin and DNA damage. Mechanism of CACF ROS such as free radical or peroxides could be a byproduct of aerobic respiration. High level of ROS can destroy the cell membrane, affects dynamic of actin cytoskeleton and causes DNA damage.
Slide 7-

ROS production in vernodalin treated human breast cancer cells were 2-4 fold higher compared to control. The basic role of the anti-cancer is the ability to stimulate ROS production, which modulate cellular redox balance leading to oxidative stress, destabilization of mitochondria then induction of apoptosis. Mitochondria role includes, once changes in MMP happen, increase the release of apoptogenic factor cytochrome c from the inner membrane space to cytoplasm.
Slide 8-

Cytochrome c, then form apoptosme with pro-caspase 9, Apaf-1 and ATP, which then activate apoptotic signals as caspase 3 and 7. Incubation with vernodalin caused time- dependant activation of caspase 9. So its increase in activity cause increase in caspase 3 and 7. caspase-3 and 7 cleave several target proteins, one of which is DNA repair enzyme PARP.
Slide 9-

Bcl-2 and Bcl-xl act as apoptotic inhibitors, but, vernodalin treatment reduced expression of the anti- apoptotic proteins. As their roles in protecting mitochondria against loss of function during apoptosis. Role of Bcl-2 in mitochondria is to block cell death by inhibiting of cytochrome c release. While Bcl-xl interact with Apaf-1 to inhibit the activation of caspase-9.
Slide 10-

ppt slide no 10 content not found
Slide 11-

ppt slide no 11 content not found
Slide 12-

ppt slide no 12 content not found
Slide 13-

Toona sinensis Kingdom: Plantae Order: Sapindales Family: Meliaceae Genus: Toona Species: T. sinensis Native in china Isolated componds are BTA and OEA.
Slide 14-

Apoptosis- inducing mechanism of BTA and OEA on human cancer cells(MCF-7, PC3) BTA and OEA could induce cancer cell apoptosis through the mitochondrial pathway, involving the expression of p53, Bax, caspase 9 and caspase 3. Mode of action P53 could induce apoptosis, if DNA damage was proved to be irreparable. BAX has been shown to be involved in p53-mediated apoptosis, p53 interacts with Bax,
Slide 15-

promoting its activation as well as its insertion into the mitochondrial membrane. bcl-2 proteins which are on mitochondrial surface, stimulate and and activate Bax , which punches holes on the membrane, causing cytochrome c leaking out . cytochrome C binds to Apaf-1, using energy from the ATP, the Apaf-1 and cytochrome C bind together to form apoptosome. Caspase 9 cleaves proteins of the mitochondrial membrane, activate caspase 3.
Slide 16-

caspase-3 is responsible for the cleavage of cellular proteins, such as cytoskeletal proteins. The Bcl-2 family divided into pro- survival members as (Bcl-2,Bcl-xl and Bcl-w) and pro- apoptotic members as (Bax,Bad and Bid). These opposing members could heterodimerize and the relative ratio of the pro- survival vs pro- apoptotic members determine whether the cell lives or dies . The pro- survival members appear to function by inhibiting the release of cytochrome c from mitochondria or by inhibiting Apaf-1 .
Slide 17-

ppt slide no 17 content not found