Arginine tagged liposomal carrier for the delivery of celastrol for ferroptosis-induced hepatocellular carcinoma therapy.

Hepatocellular carcinoma (HCC) is a predominant malignant liver tumor that cannot be efficiently treated because of poor response, toxicity, and drug resistance. Ferroptosis is an iron-dependent way of cell death associated with abnormal intracellular lipid metabolism. Celastrol (Cel) has the ability to inhibit the progression of HCC by regulating multiple signaling pathways and induce ferroptosis.

NaHS modulates astrocytic EAAT2 expression to impact SNI-induced neuropathic pain and depressive-like behaviors.

The potential role of hydrogen sulfide (HS) in the modulation of neuropathic pain is increasingly recognized. This study investigated the therapeutic effect of intraperitoneal injection of the HS donor sodium hydrosulfide (NaHS) on neuropathic pain. Utilizing the spared nerve injury (SNI) model in mice, the research investigates the role of astrocytes and the excitatory neurotransmitter glutamate in chronic pain.

Integrating Network Pharmacology with in vitro Experiments to Validate the Efficacy of Celastrol Against Hepatocellular Carcinoma Through Ferroptosis.

Background: As a traditional Chinese medicine monomer derived from Tripterygium wilfordii Hook.f. with potential anticancer activity, celastrol can induce ferroptosis in hepatic stellate cells and inhibit their activation to alleviate liver fibrosis.

Celastrol induces ferroptosis by suppressing RRM2 in hepatocellular carcinoma.

Introduction And Objectives: Ferroptosis is a novel form of cell death driven by iron dependence and lipid peroxidation, presenting a promising potential as an innovative strategy for cancer treatment. Celastrol (Cel) is particularly effective in inducing ferroptosis, but its molecular mechanism remains unclear. The study aims to elucidate the potential mechanism through both in vitro and in vivo experiments.

Ferroptosis inhibitors reduce celastrol toxicity and preserve its insulin sensitizing effects in insulin resistant HepG2 cells.

Objective: Research has shown that celastrol can effectively treat a variety of diseases, yet when passing a certain dosage threshold, celastrol becomes toxic, causing complications such as liver and kidney damage and erythrocytopenia, among others. With this dichotomy in mind, it is extremely important to find ways to preserve celastrol's efficacy while reducing or preventing its toxicity.

Methods: In this study, insulin-resistant HepG2 (IR-HepG2) cells were prepared using palmitic acid and used for in vitro experiments.

VX-765 Alleviates Circadian Rhythm Disorder in a Rodent Model of Traumatic Brain Injury Plus Hemorrhagic Shock and Resuscitation.

Severe traumatic brain injury (TBI) can result in persistent complications, including circadian rhythm disorder, that substantially affect not only the injured people, but also the mood and social interactions with the family and the community. Pyroptosis in GFAP-positive astrocytes plays a vital role in inflammatory changes post-TBI. We determined whether VX-765, a low molecular weight caspase-1 inhibitor, has potential therapeutic value against astrocytic inflammation and pyroptosis in a rodent model of TBI plus hemorrhagic shock and resuscitation (HSR).

Characterization of Global Research Trends and Prospects on Moyamoya Disease: Bibliometric Analysis.

Background: Moyamoya disease (MMD) is a rare cerebrovascular disease in neurology. This study investigates the literature related to MMD from its discovery to the present and identifies research levels, achievements, and trends.

Methods: All publications on MMD from its discovery to present were downloaded from the Web of Science Core Collection on September 15, 2022 and bibliometric analyses were visualized by HistCite Pro, VOSviewer, Scimago Graphica, CiteSpace, and R language.

More advantages of trocar compared than steel needle in deep venipuncture catheterization.

Background: Deep venipuncture catheterization is widely used in clinical anesthesia. However, it is worth thinking about how to improve the rate of successful catheter insertion, and relieve patients' discomfort. This paper aimed to compare the clinical advantages between trocar and steel needle.

Melatonin mitigates traumatic brain injury-induced depression-like behaviors through HO-1/CREB signal in rats.

In addition to significant antioxidant properties, melatonin exhibits neuroprotective effects against various neurological diseases including traumatic brain injury (TBI) and ischemic stroke. Several potential mechanisms have been reported in the neuroprotection of melatonin among patients with TBI. Notably, the heme oxygenase-1 (HO-1)/cAMP response element-binding protein (CREB) signaling pathway is implicated in the development of a depressive state.

Melatonin alleviates traumatic brain injury-induced anxiety-like behaviors in rats: Roles of the protein kinase A/cAMP-response element binding signaling pathway.

Melatonin is a hormone produced by the pineal gland. Given its capabilities of neuroprotection and low neurotoxicity, melatonin could be a therapeutic strategy for traumatic brain injury (TBI). The present study was conducted to determine the neuroprotective effects of melatonin on TBI-induced anxiety and the possible molecular mechanism.

Androgen is responsible for enhanced susceptibility of melatonin against traumatic brain injury in females.

Background: Numerous publications have demonstrated that melatonin administration is associated with mortality reduction and improvement in neurological outcomes after traumatic brain injury (TBI). However, there are significant sex differences in several diseases associated with melatonin. We aimed to determine whether androgen was responsible for enhanced susceptibility of melatonin against TBI in females, as well as potential molecular mechanisms.

Low-Dose, Early Fresh Frozen Plasma Transfusion Therapy After Severe Trauma Brain Injury: A Clinical, Prospective, Randomized, Controlled Study.

Background: To investigate role of Low-dose, Early Fresh frozen plasma Transfusion (LEFT) therapy in preventing perioperative coagulopathy and improving long-term outcome after severe traumatic brain injury (TBI).

Methods: A prospective, single-center, parallel-group, randomized trial was designed. Patients with severe TBI were eligible.

Carbon monoxide-releasing molecule-3 protects against cortical pyroptosis induced by hemorrhagic shock and resuscitation via mitochondrial regulation.

Objective: Carbon monoxide (CO) releasing molecule (CORM)-3, a water-soluble CORM, has protective effects against inflammatory and ischemia/reperfusion injury. We determined the effect of CORM-3 against neuronal pyroptosis in a model of hemorrhagic shock and resuscitation (HSR) in rats via mitochondrial regulation.

Methods: Rats were treated with CORM-3 (4 mg/kg) in vitro after HSR.