Preventive Effect of Royal Jelly and 10-HDA on Skin Damage in Diabetic Mice through Regulating Keratinocyte Wnt/β-Catenin and Pyroptosis Pathway.

The objective of this study is to elucidate how Royal jelly (RJ) and 10-hydroxy-2-decanoic acid (10-HDA) prevents diabetic skin dysfunction by modulating the pyroptosis pathway. Type 2 diabetes models are induced by fat diet consumption and low dose of streptozotocin (STZ) in C57BL/6J mice and treated with RJ (100 mg kg day) and 10-HDA, the major lipid component of royal jelly (100 mg kg day) for 28 weeks. The results show that serum concentrations of glucose and triglyceride are significantly lower in the RJ group or 10-HDA than diabetes mellitus (DM) group.

Upregulation of RAB7 is related to neuronal pyroptosis after spinal cord injury in rats.

Rab7 belongs to the Ras small GTPase superfamily, and abnormal expression of Rab7 can cause neuropathy and lipid metabolism diseases. Studies have shown that Rab7 plays a crucial role in the inner membrane translocase. However, the role of Rab7 in the regulatory mechanisms of cell survival in spinal cord injury remains unknown.

The Role of Copper Homeostasis in Brain Disease.

In the human body, copper is an important trace element and is a cofactor for several important enzymes involved in energy production, iron metabolism, neuropeptide activation, connective tissue synthesis, and neurotransmitter synthesis. Copper is also necessary for cellular processes, such as the regulation of intracellular signal transduction, catecholamine balance, myelination of neurons, and efficient synaptic transmission in the central nervous system. Copper is naturally present in some foods and is available as a dietary supplement.

Surface-fill HS-releasing silk fibroin hydrogel for brain repair through the repression of neuronal pyroptosis.

Traumatic brain injury (TBI) remains the major cause of disability and mortality worldwide due to the persistent neuroinflammation and neuronal death induced by TBI. Among them, pyroptosis, a specific type of programmed cell death (PCD) triggered by inflammatory signals, plays a significant part in the pathological process after TBI. Inhibition of neuroinflammation and pyroptosis is considered a possible strategy for the treatment of TBI.

Implantation of injectable SF hydrogel with sustained hydrogen sulfide delivery reduces neuronal pyroptosis and enhances functional recovery after severe intracerebral hemorrhage.

Hydrogen sulfide (HS), an important endogenous signaling molecule, plays an important neuroprotective role in the central nervous system. However, there is no ideal delivery material or method involving the sustained and controlled release of HS for clinical application in brain diseases. Silk fibroin (SF)-based hydrogels have become a potentially promising strategy for local, controlled, sustained drug release in the treatment of various disorders.

Silk Fibroin Hydrogels Could Be Therapeutic Biomaterials for Neurological Diseases.

Silk fibroin, a natural macromolecular protein without physiological activity, has been widely used in different fields, such as the regeneration of bones, cartilage, nerves, and other tissues. Due to irrevocable neuronal injury, the treatment and prognosis of neurological diseases need to be investigated. Despite attempts to propel neuroprotective therapeutic approaches, numerous attempts to translate effective therapies for brain disease have been largely unsuccessful.

A hydrogen sulphide-responsive and depleting nanoplatform for cancer photodynamic therapy.

Hydrogen sulfide (HS) as an important biological gasotransmitter plays a pivotal role in many physiological and pathological processes. The sensitive and quantitative detection of HS level is therefore crucial for precise diagnosis and prognosis evaluation of various diseases but remains a huge challenge due to the lack of accurate and reliable analytical methods in vivo. In this work, we report a smart, HS-responsive and depleting nanoplatform (ZNNPs) for quantitative and real-time imaging of endogenous HS for early diagnosis and treatment of HS-associated diseases.

The Role of Mitophagy in Regulating Cell Death.

Mitochondria are multifaceted organelles that serve to power critical cellular functions, including act as power generators of the cell, buffer cytosolic calcium overload, production of reactive oxygen species, and modulating cell survival. The structure and the cellular location of mitochondria are critical for their function and depend on highly regulated activities such as mitochondrial quality control (MQC) mechanisms. The MQC is regulated by several sets of processes: mitochondrial biogenesis, mitochondrial fusion and fission, mitophagy, and other mitochondrial proteostasis mechanisms such as mitochondrial unfolded protein response (mtUPR) or mitochondrial-derived vesicles (MDVs).