Exploring the GSTP1 inhibition potential of photosensitizer compounds for enhanced cancer treatment in photodynamic therapy.

Photodynamic therapy (PDT) has gained considerable attention in cancer treatment due to its non-invasive nature and the ability of photosensitizers to generate reactive oxygen species upon light activation, leading to tumor destruction. Glutathione S-transferase P1 (GSTP1) is a key enzyme in chemotherapy resistance, often overexpressed in various cancers, and its inhibition of GSTP1 presents a promising strategy to enhance cancer treatment. This study is aimed at assessing the potential of prominent photosensitizers as GSTP1 inhibitors through molecular docking analysis to strengthen the efficacy of PDT.

Eyelid skin and fibroadipose tissue MMP-1, MMP-3, TNF-α, and IL-6 levels in patients with inactive moderate-to-severe Graves' orbitopathy.

Purpose: To evaluate matrix metalloprotease-1 (MMP-1), matrix metalloprotease-3 (MMP-3), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) levels in the eyelid skin and fibroadipose tissue in patients with inactive moderate-to-severe Graves' orbitopathy (GO).

Methods: This prospective study included 23 patients with inactive moderate-to-severe GO who underwent upper blepharoplasty and medial fat excision, and 22 age- and sex-matched healthy subjects. MMP-1, MMP-3, TNF-α, and IL-6 levels in the skin and fibroadipose tissue obtained during surgery were measured using the ELISA method.

Butyrylcholinesterase in lipid metabolism: A new outlook.

Cholinesterase enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) are traditionally associated with the termination of acetylcholine mediated neural signaling. The fact that these ubiquitous enzymes are also found in tissues not involved in neurotransmission has led to search for alternative functions for these enzymes. Cholinesterases are reported to be involved in many lipid related disease states.

Novel activity of human BChE: Lipid hydrolysis.

Acetylcholinesterase and butyrylcholinesterase (BChE) typically hydrolyze the neurotransmitter acetylcholine. The multifunctional enzyme BChE is associated with lipid metabolism through an undefined mechanism. Based on lipid-related studies and by comparing the structural similarities between lipases and BChE we postulated that the association of BChE with lipid metabolism could occur through hydrolytic activity.

Altered levels of variant cholinesterase transcripts contribute to the imbalanced cholinergic signaling in Alzheimer's and Parkinson's disease.

Acetylcholinesterase and butyrylcholinesterase (AChE and BChE) are involved in modulating cholinergic signaling, but their roles in Alzheimer's and Parkinson's diseases (AD and PD) remain unclear. We identified a higher frequency of the functionally impaired BCHE-K variant (rs1803274) in AD and PD compared to controls and lower than in the GTEx dataset of healthy individuals ( = 651); in comparison, the prevalence of the 5'-UTR (rs1126680) and intron 2 (rs55781031) single-nucleotide polymorphisms (SNPs) of BCHE and ACHE's 3'-UTR (rs17228616) which disrupt AChE mRNA targeting by miR-608 remained unchanged. qPCR validations confirmed lower levels of the dominant splice variant encoding the "synaptic" membrane-bound ACHE-S in human post-mortem superior temporal gyrus samples from AD and in substantia nigra (but not amygdala) samples from PD patients ( = 79, = 67) compared to controls, potentially reflecting region-specific loss of cholinergic neurons.

Melatonin is effective in attenuating cisplatin-induced neurotoxicity.

Cisplatin (Cis) is a chemotherapeutic agent that has many side effects. Neurotoxicity is one of the most important of these side effects. Oxidative stress and neuroinflammation are the best-known mechanisms in the pathogenesis of neurotoxicity development.

cAMP/PKA-CREB-BDNF signaling pathway in hippocampus of rats subjected to chemically-induced phenylketonuria.

Phenylketonuria (PKU) is an inborn error disease in phenylalanine metabolism resulting from defects in the stages of converting phenylalanine to tyrosine. Although the pathophysiology of PKU is not elucidated yet, the toxic effect of phenylalanine on the brain causes severe mental retardation. In relation to learning and memory, the hippocampal PKA / CREB / BDNF pathway may play a role in learning deficits in PKU patients.

Composite nanofibers incorporating alpha lipoic acid and atorvastatin provide neuroprotection after peripheral nerve injury in rats.

Despite the new treatment strategies within the last 30 years, peripheral nerve injury (PNI) is still a worldwide clinical problem. The incidence rate of PNIs is 1 in 1000 individuals per year. In this study, we designed a composite nanoplatform for dual therapy in peripheral nerve injury and investigated the in-vivo efficacy in rat sciatic nerve crush injury model.

Data the DEHP induced changes on the trace element and mineral levels in the brain and testis tissues of rats.

Di (2-ethylhexyl) phthalate (DEHP) is used as plasticizer in the industry and belongs to the phthalate family which can induce tissue damage including kidney, liver, and testis as a result of elevated oxidative stress levels. Glutathione reductase (GR), Glucose-6-phosphate dehydrogenase (G6PD), glutathione S-transferase (GST), 6-phosphogluconate dehydrogenase (6PGD), enzyme activities, trace element and mineral levels were evaluated in the brain and testis tissue samples. Our data revealed that, antioxidant enzyme activities in the brain and testis samples were statistically insignificant in the DEHP administered groups compared to the control group except 400 mg/kg/day DEHP dose group in the testis samples.

Effects of Timolol Treatment on Pancreatic Antioxidant Enzymes in Streptozotocin-induced Diabetic Rats: An Experimental and Computational Study.

Background: The study aimed to investigate whether timolol-treatment has a beneficial effect on pentose phosphate pathway enzyme activities such as glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGDH) enzyme activities and cAMP level in streptozotocin-induced diabetic rats in pancreatic tissues.

Methods: Diabetes was induced by streptozotocin (STZ) in 3-month old male Wistar rats. The diabetic rats were treated with timolol (5 mg/kg body weight, for 12 weeks) while the control group received saline.

Antioxidant SMe1EC2 modulates pentose phosphate pathway and glutathione-dependent enzyme activities in tissues of aged diabetic rats.

The pentose phosphate pathway and glutathione-associated metabolism are the main antioxidant cellular defense systems. This study investigated the effects of the powerful antioxidant SMe1EC2 (2-ethoxycarbonyl-8-methoxy-2,3,4,4a,5,9b-hexahydro-1H-pyrido[4,3-b] indolinium dichloride) on pentose phosphate pathway (PPP) and glutathione-dependent enzyme activities in aged diabetic and aged matched control rats. Diabetes was induced by streptozotocin injection in rats aged 13-15 months.

Impact of the Di(2-Ethylhexyl) Phthalate Administration on Trace Element and Mineral Levels in Relation of Kidney and Liver Damage in Rats.

Di(2-ethylhexyl) phthalate (DEHP) is a widely used synthetic polymer in the industry. DEHP may induce reproductive and developmental toxicity, obesity, carcinogenesis and cause abnormal endocrine function in both human and wildlife. The aim of this study was to investigate trace element and mineral levels in relation of kidney and liver damage in DEHP-administered rats.

Butyrylcholinesterase expression is regulated by fatty acids in HepG2 cells.

Butyrylcholinesterase (BChE) is mostly associated with the detoxification of xenobiotics. In this study to analyze the involvement of BChE in lipid metabolism, linoleic acid (LA) and α-linolenic acid (ALA) were applied to HepG2 cells along with expression of wild type human BChE. After 48 h of these treatments WST-1 cell proliferation assay, FACS analysis, RT-PCR, Oil Red O staining and activity assays were performed.

Flaxseed Protects Against Diabetes-Induced Glucotoxicity by Modulating Pentose Phosphate Pathway and Glutathione-Dependent Enzyme Activities in Rats.

This study investigated the effects of flaxseed (Linum usitatissimum L.) intake on general metabolism, pentose phosphate pathway (PPP) and glutathione-dependent enzymes in diabetic rats. Diabetes was induced by streptozotocin injection (40 mg/kg, i.

Long-term treatment with a beta-blocker timolol attenuates renal-damage in diabetic rats via enhancing kidney antioxidant-defense system.

The factors with increasing diabetes-prevalence lead to significant global increases in chronic kidney disease. Since hyperglycemia generates more ROS and attenuates cellular antioxidant-defense mechanisms, numerous studies demonstrated that hyperglycemia-induced oxidative stress played a major role in the extracellular matrix expansion in tissues. Although no direct relation between activation of beta-adrenergic (β-AR) system and kidney disease in diabetes and since β-blockers demonstrate marked beneficial effects due to their scavenging free radicals and/or acting as an antioxidant in diabetic animal studies, the eventual objective of the present study was to determine whether timolol-treatment of streptozotocin-induced diabetic rats (5 mg/kg, daily following diabetes-induction, for 12-week) has advantage to prevent hyperglycemia-induced renal-damage via enhancing the depressed antioxidant defense in the kidney.