Eskandar Qaed’s research while affiliated with Lanzhou University and other places

Breast cancer remains one of the leading causes of cancer-related deaths among women worldwide. Genistein (Gen), a phytoestrogen soy isoflavone, has emerged as a promising agent in the prevention and treatment of breast cancer due to its ability to function as a natural selective estrogen receptor modulator (SERM). This review explores the multifaceted mechanisms through which Gen and its derivatives exert their anticancer effects, including modulation of the PI3K/Akt signaling pathway, regulation of apoptosis, inhibition of angiogenesis, and impacts on DNA methylation and enzyme functions. We discuss the dual roles of Gen in both enhancing and inhibiting estrogen receptor (ER)-dependent pathways., highlighting its complex interactions with ERα and ERβ. Furthermore, the review examines the synergistic effect of combining Gen with conventional chemotherapeutic agents such as doxorubicin, cisplatin, and selenium, as well as other natural compounds like lycopene. Clinical studies suggest that while isoflavones may not significantly influence breast cancer progression in general, the high consumption of soy isoflavones is associated with reduced recurrence rates in breast cancer survivors. Importantly, Gen’s ability to modulate key signaling pathways and enhance the efficacy of existing treatments improves its potential as a valuable adjunct in breast cancer therapy. In conclusion, Gen and its derivatives offer a novel and promising approach for treatment of breast cancer. Continued research into their mechanisms of action and clinical applications will be essential in optimizing their therapeutic potential and translating these findings into effective clinical interventions.

Phosphocreatine (PCr) has been shown to have a cardio-protective effect during cardiopulmonary resuscitation (CPR). However, little is known about its impact on atherosclerosis. In this study, we firstly evaluated the pharmacological effects of PCr on antioxidative defenses and mitochondrial protection against hydrogen peroxide (H 2 O 2 ) induced human umbilical vascular endothelial cells (HUVECs) damage. Then we investigated the hypolipidemic and antioxidative effects of PCr on hyperlipidemic rat model. Via in vitro studies, H 2 O 2 significantly reduced cell viability and increased apoptosis rate of HUVECs, while pretreatment with PCr abolished its apoptotic effect. PCr could reduce the generation of ROS induced by H 2 O 2 . Moreover, PCr could increase the activity of SOD and the content of NO, as well as decrease the activity of LDH and the content of MDA. PCr could also antagonize H 2 O 2 -induced up-regulation of Bax, cleaved-caspase3, cleaved-caspase9, and H 2 O 2 -induced down-regulation of Bcl-2 and p-Akt/Akt ratio. In addition, PCr reduced U937 cells’ adhesion to H 2 O 2 -stimulated HUVECs. Via in vivo study, PCr could decrease MDA, TC, TG and LDL-C levels in hyperlipidemic rats. Finally, different-concentration PCr could increase the leaching of TC, HDL, and TG from fresh human atherosclerotic plaques. In conclusion, PCr could suppress H 2 O 2 -induced apoptosis in HUVECs and reduce hyperlipidemia through inhibiting ROS generation and modulating dysfunctional mitochondrial system, which might be an effective new therapeutic strategy to further prevent atherosclerosis.

The most prevalent chronic consequence of diabetes mellitus is diabetic retinopathy (DR), a clinically microvascular disease characterized by damage to retinal capillaries with subsequent visual deterioration or blindness. DR is mainly attributed to hyperglycemia-induced retinal microvascular damage, however, emerging research has demonstrated that it is intimately linked to mitochondrial energy shortage and raises the generation of reactive emerging research has demonstrated that it is intimately linked to mitochondrial energy shortage and raises the generation of reactive oxygen species (ROS). This study is aimed to develop and investigate methods to safeguard DR membrane composition, such as regaining methods to safeguard DR membrane composition, such as regaining mitochondrial function. Controlling for hyperglycemia cannot reverse the pathologic changes induced by diabetes in the retinal mitochondria. In mitochondria damaged by hyperglycemia, we proposed that phosphocreatine (PCr) might enhance oxidative phosphorylation and electron transport capability. Similarly, we anticipated estimating PCr's protection against DR via the JAK2/STAT3 signaling pathway. PCr has a crucial metabolic function in DR cells, which includes controlling the intracellular content of ATP. Rat mitochondria and RGC-5 cells were evaluated for capacity using high-resolution respirometry (HRR). The expression of JAK2/STAT3 signaling pathways and apoptotic proteins were detected using western blotting. We assessed ROS production and mitochondrial membrane potential (MMP) in Wistar male rats with streptozotocin induced-diabetes. In this study, we found that PCr had protective effects against DR injury by boosting mitochondrial bioenergetics and preventing DR by easing the symptoms of diabetes and improving biochemical indicators. Additionally, PCr decreased the expression of Bax, cleaved caspase 3, cleaved caspase 9, as well as the JAK2/STAT3 signaling pathway while increasing the expression of Bcl-2, caspase 3, and caspase 9 proteins. In Conclusions when exposed to oxidative stress caused by hyperglycemia, PCr improves mitochondrial activity and has antiapoptotic effects in vivo and in vitro through the JAK2/STAT3 signaling pathway. These findings suggest that PCr is a potentially effective therapeutic approach for diabetic retinopathy.