KZA Drug Other Than Cancer

Starting a new threat for presentation of research....which features studies in PI3K Pathway Inhibition (most agree that is what the KZA drug does)......other than in the treatment of cancer.

Obviously the whole intention to to inform...... but it should highlight a rather bizarre circumstance here, given the usual credible research that comes from these reputable institutions around the world.

Anybody can post whatever they like here (are they having a nice day ?)......but in particular when I post here in the future - very strict criteria, will be used to make the cut for research into this thread. I can maybe 6 or 7 human diseases can meet the criteria, but lets do one at a time. (Not a typo)

Criteria Used to Be Included Here (Myself at Least) :

Must Make Reference to Use of Other PI3K Drugs in Studies

Easy to Understand / Short to the Point

No More than 12 Months Old

Specific to CNS/ Brain

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Are people interested -if somebody else posted, I would be. Lets start with Parkinson's (although last week we had Alzimers -under a different thread). Plenty more to come - needle
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TRIM3 attenuates apoptosis in Parkinson's disease via activating PI3K/AKT signal pathway Wenwen Dong1,*, Bei Luo1,*, Chang Qiu1 , Xu Jiang2 , Bo Shen2 , Li Zhang2 , Weiguo Liu2 , Wenbin Zhang1 1Department of Functional Neurosurgery, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China 2Neurology Department, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China *Co-first authors Correspondence to: Wenbin Zhang; email: [email protected] Keywords: PD, TRIM3, apoptosis, ROS, PI3K/AKT Received: March 1, 2020 Accepted: October 15, 2020 Published: November 30, 2020

ABSTRACT This article aims to study tripartite motif-containing protein 3 (TRIM3) effects on Parkinson's disease (PD). TRIM3 expression in venous blood of PD patients was detected by qRT-PCR. PD mouse model and PD SH-SY5Y cell model were constructed. PD cells were treated by LY294002 (a PI3K inhibitor). The apoptosis of PD mouse midbrain was detected. Glutathione (GSH) and superoxide dismutase (SOD) level in PD cells and mice midbrain was analyzed. Intracellular reactive oxygen species (ROS) and MMP were detected. The effect of TRIM3 on cell viability, apoptosis and PI3K/AKT signal pathway were analyzed. As a result, TRIM3 expression in venous blood of PD patients was decreased. TRIM3 up-regulation in PD mouse decreased midbrain tissues apoptosis. TRIM3 up-regulation increased GSH and SOD levels in PD mice midbrain tissues and PD cells. TRIM3 up-regulation in PD cells prominently reduced ROS and MMP. TRIM3 up-regulation increased PD cells viability and decreased apoptosis. TRIM3 up-regulation in PD cells elevated Bcl-2 protein expression and weakened Bax, Cleavedcaspase 3 and Cleaved-caspase 9 proteins expression. TRIM3 up-regulation increased p-PI3K/PI3K and pAKT/AKT ratio. PI3K inhibitor treatment reversed the inhibitory effect of TRIM3 up-regulation on PD cells apoptosis. Thus, TRIM3 might attenuate apoptosis in PD via activating PI3K/AKT signal pathway.