CD36-mediated ROS/PI3K/AKT signaling pathway exacerbates cognitive impairment in APP/PS1 mice after noise exposure.

There is an association between noise exposure and cognitive impairment, and noise may have a more severe impact on patients with Alzheimer's disease (AD) and mild cognitive impairment; however, the mechanisms need further investigation. This study used the classic AD animal model APP/PS1 mice to simulate the AD population, and C57BL/6J mice to simulate the normal population. We compared their cognitive abilities after noise exposure, analyzed changes in Cluster of Differentiation (CD) between the two types of mice using transcriptomics, identified the differential CD molecule: CD36 in APP/PS1 after noise exposure, and used its pharmacological inhibitor to intervene to explore the mechanism by which CD36 affects APP/PS1 cognitive abilities.

Thioredoxin-1 Protects Neurons Through Inhibiting NLRP1-Mediated Neuronal Pyroptosis in Models of Alzheimer's Disease.

Alzheimer's disease (AD) is the most common neurodegenerative disease all over the world. In the last decade, accumulating proofs have evidenced that neuroinflammation is intimately implicated in the pathogenesis of AD and activation of NOD-like receptor family pyrin domain-containing 1 (NLRP1) inflammasome can induce neuronal pyroptosis and in turn lead to neuronal loss in AD. Thioredoxin-1 (Trx-1), a multifunctional molecule with anti-inflammation in human tissues, displays crucial neuroprotective roles in AD.

NLRP3/1-mediated pyroptosis: beneficial clues for the development of novel therapies for Alzheimer's disease.

The inflammasome is a multiprotein complex involved in innate immunity that mediates the inflammatory response leading to pyroptosis, which is a lytic, inflammatory form of cell death. There is accumulating evidence that nucleotide-binding domain and leucine-rich repeat pyrin domain containing 3 (NLRP3) inflammasome-mediated microglial pyroptosis and NLRP1 inflammasome-mediated neuronal pyroptosis in the brain are closely associated with the pathogenesis of Alzheimer's disease. In this review, we summarize the possible pathogenic mechanisms of Alzheimer's disease, focusing on neuroinflammation.

Thioredoxin-1 decreases alpha-synuclein induced by MPTP through promoting autophagy-lysosome pathway.

Parkinson's disease (PD) is characterized by the formation of Lewy body in dopaminergic neurons in the substantia nigra pars compacta (SNpc). Alpha-synuclein (α-syn) is a major component of Lewy body. Autophagy eliminates damaged organelles and abnormal aggregated proteins.

Corrigendum: Advances in the roles of glycyrrhizic acid in cancer therapy.

[This corrects the article DOI: 10.3389/fphar.2023.

Advances in the roles of glycyrrhizic acid in cancer therapy.

Since the first 70 years of reporting cancer chemotherapy, malignant tumors have been the second most common cause of death in children and adults. Currently, the commonly used anti-cancer methods include surgery, chemotherapy, radiotherapy, and immunotherapy. Although these treatment methods could alleviate cancer, they lead to different forms of side effects and have no particularly significant effect on prolonging the patients' life span.

Thioredoxin-1 inhibits the activation of IRE1 by targeting Hsp90/p-Cdc37 chaperone complex in Parkinson disease.

Endoplasmic reticulum stress is implicated in the etiopathogenesis of Parkinson disease (PD). Our previous study has revealed that thioredoxin-1 (Trx-1) attenuated IRE1 activation in 1-methyl-4-phenylpyridinium ion (MPP)/1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD models. However, its exact mechanism has been largely unclear.

Thioredoxin-1 Promotes Mitochondrial Biogenesis Through Regulating AMPK/Sirt1/PGC1α Pathway in Alzheimer's Disease.

Alzheimer's disease (AD) is the most common neurodegenerative disease. Increasing studies suggest that mitochondrial dysfunction is closely related to the pathogenesis of AD. Thioredoxin-1 (Trx-1), one of the major redox proteins in mammalian cells, plays neuroprotection in AD.

Estrogen Protects against Renal Ischemia-Reperfusion Injury by Regulating Th17/Treg Cell Immune Balance.

Inflammation is a critical mediator of renal ischemia-reperfusion (I/R) injury (IRI), and T lymphocytes exert a key role in the renal IRI-induced inflammation. Connexin 43 (Cx43) is related to the maintenance of T lymphocyte homeostasis. Various preclinical researches have reported that estrogen is a renoprotective agent based on its anti-inflammatory potential.

Advances in the Functions of Thioredoxin System in Central Nervous System Diseases.

The thioredoxin system comprises thioredoxin (Trx), thioredoxin reductase (TrxR), and nicotinamide adenine dinucleotide phosphate, besides an endogenous Trx inhibitor, the thioredoxin-interacting protein (TXNIP). The Trx system plays critical roles in maintaining the redox homeostasis in the central nervous system (CNS), in which oxidative stress damage is prone to occurrence due to its high-energy demand. Increasing studies have demonstrated that the expression or activity of Trx/TrxR is usually decreased and that TXNIP expression is increased in patients with CNS diseases, including neurodegenerative diseases, cerebral ischemia, traumatic brain injury, and depression, as well as in their cellular and animal models.

Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases.

Panax ginseng and Panax notoginseng, two well-known herbs with enormous medical value in Asian countries, have a long usage history in China for the therapy of some diseases, such as stroke. Ginsenoside Rb1 is one of most important active ingredients in Panax ginseng and Panax notoginseng. In the last two decades, more attention has focused on ginsenoside Rb1 as an antioxidative, anti-apoptotic and anti-inflammatory agent that can protect the nervous system.

Thioredoxin-1 inhibits amyloid-β-induced activation of NLRP1/caspase-1/GSDMD pyroptotic pathway in PC12 cells.

Background: Alzheimer's disease (AD), the most common neurodegenerative disease, is charactered by these accepted pathological features, such as β-amyloid (Aβ) plaques outside the neurons and neurofibrillary tangles inside the neurons. In recent years, several studies have demonstrated that pyroptosis is associated with the development of AD process. However, whether Aβ induces pyroptosis is still unclear.

Advances in forensic diagnosis of electric shock death in the absence of typical electrical marks.

Electrical injury is a relatively uncommon but potentially devastating form of multi-system injury with high morbidity and mortality. In common electric injury cases, it is usually difficult to find characteristic changes of electric injury in major organs by using routine histopathological test methods unless there are landmark traces of electric injury, known as electric marks. How to determine electric shock death, especially in the absence of typical electrical marks on the body surface in some cases (which account for about two-thirds of electric injury cases), remains a challenging problem in forensic practice.

Ovarian dysgerminoma with pseudo-Meigs syndrome: A case report.

Rationale: Dysgerminoma is a rare malignant tumor of the ovary, more frequently occurring in young women. The main signs of pseudo-Meigs syndrome (PMS) are ascites and hydrothorax accompanying benign or malignant ovarian tumors (no fibroma or fibroma-like tumor).

Patient Concerns: A 19-year-old woman with fever and chest tightness for 2 days.

Liver extracellular matrix hydrogel-based three-dimensional culture system of HepG2 cells to enhance cancer stem cell properties.

Both extracellular matrix (ECM) components and three-dimensional (3D) structure play important roles in the expression and maintenance of cancer stem cell (CSC) properties. Considering the excellent biophysical and biochemical properties of hydrogels, the objective of this study was to develop a 3D cell culture system based on liver ECM hydrogel (LEMH) to enhance CSC properties. Results showed that LEMH was devoid of cellular materials but contained the main components of the liver ECM.

Advances in Stem Cells Transplantation for the Therapy of Parkinson's Disease.

Parkinson's disease (PD) is a common neurodegenerative disease and is a major culprit that harms the health of elderly people. The main pathological feature is the progressive loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. The current mainstream therapeutic strategies include surgical treatment and medicine substitute therapy.

The Potential Roles of Redox Enzymes in Alzheimer's Disease: Focus on Thioredoxin.

Alzheimer's disease (AD) is the most common neurodegenerative diseases. Increasing studies have demonstrated the critical importance for redox proteins mediating neuronal protection in models of AD. This review briefly describes some of the risk factors contributing to AD, specifically highlighting the important roles of oxidative stress in the pathology of AD.

Exploration of sensory and spinal neurons expressing gastrin-releasing peptide in itch and pain related behaviors.

Gastrin-releasing peptide (GRP) functions as a neurotransmitter for non-histaminergic itch, but its site of action (sensory neurons vs spinal cord) remains controversial. To determine the role of GRP in sensory neurons, we generated a floxed Grp mouse line. We found that conditional knockout of Grp in sensory neurons results in attenuated non-histaminergic itch, without impairing histamine-induced itch.

Morphine Addiction and Oxidative Stress: The Potential Effects of Thioredoxin-1.

Long-term administration of morphine for the management of chronic pain will result in tolerance to its analgesic effect and could even cause drug dependence. Numerous studies have demonstrated significant redox alteration in morphine dependence and addiction. Thioredoxin-1 (Trx-1) play important roles in controlling the cellular redox balance.

The role of thioredoxin system in cancer: strategy for cancer therapy.

Purpose: Cancer, a major public health problem, exhibits significant redox alteration. Thioredoxin (Trx) system, including Trx and Trx reductase (TrxR), as well as Trx-interacting protein (TXNIP) play important roles in controlling the cellular redox balance in cancer cells. In most cancers, Trx and TrxR are usually overexpressed and TXNIP is underexpressed.

Thioredoxin as a Therapeutic Target in Cerebral Ischemia.

Background: Cerebral ischemia is a common cause of disability and death. Ischemic brain injury results from complex pathological processes, including oxidative stress, inflammation, and apoptosis. Thioredoxin( Trx) is an important multifunctional protein, which regulates cellular redox status.