Nuclear Receptor PPARα as a Therapeutic Target in Diseases Associated with Lipid Metabolism Disorders.

Lipid metabolic diseases have substantial morbidity and mortality rates, posing a significant threat to human health. PPARα, a member of the peroxisome proliferator-activated receptors (PPARs), plays a crucial role in lipid metabolism and immune regulation. Recent studies have increasingly recognized the pivotal involvement of PPARα in diverse pathological conditions. This comprehensive review aims to elucidate the multifaceted role of PPARα in metabolic diseases including liver diseases, diabetes-related diseases, age-related diseases, and cancers, shedding light on the underlying molecular mechanisms and some regulatory effects of natural/synthetic ligands of PPARα. By summarizing the latest research findings on PPARα, we aim to provide a foundation for the possible therapeutic exploitation of PPARα in lipid metabolic diseases.

Curcumin derived from medicinal homologous foods: its main signals in immunoregulation of oxidative stress, inflammation, and apoptosis.

It has been for thousands of years in China known medicinal homologous foods that can be employed both as foods and medicines to benefit human and animal health. These edible herbal materials perform divert roles in the regulation of metabolic disorders, cancers, and immune-related diseases. Curcumin, the primary component derived from medicinal homologous foods like curcuma longa rhizome, is reported to play vital actions in organic activities, such as the numerous pharmacological functions including anti-oxidative stress, anti-inflammation and anti/pro-apoptosis in treating various diseases. However, the potential mechanisms of curcumin-derived modulation still need to be developed and attract more attention worldwide. Given that these signal pathways are enrolled in important bioactive reactions, we collected curcumin's last achievements predominantly on the immune-regulation signals with the underlying targetable strategies in the last 10 years. This mini-review will be helpful to accelerate curcumin and other extracts from medicinal homologous foods use in future human clinical applications.

iTRAQ-based quantitative proteomic analysis of the therapeutic effects of 2% hydrogen gas inhalation on brain injury in septic mice.

Sepsis encephalopathy (SAE) has a high incidence and mortality rate in patients with sepsis; however, there is currently no effective treatment. Our previous studies have reported that 2% hydrogen (H2) gas inhalation had a protective effect on sepsis and SAE; however, the specific mechanism have not been fully elucidated. In the current study, male Institute of Cancer Research mice were either used to create the cecal ligation and puncture (CLP) model or for sham surgery, followed by 2% H2 gas inhalation for 60 min beginning at 1 and 6 h following sham or CLP surgeries. The isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomics combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, hematoxylin and eosin (H&E) staining, Nissl staining, and western blot analysis were used to investigate the effects of H2 on brain injury in mice with sepsis. The results of the H&E, and Nissl staining indicated that the CLP mice had a significant brain injury, which was characterized by aggravated pathological damage and was alleviated by 2% H2 inhalation. Quantitative proteomics based on iTRAQ combined with LC-MS/MS analysis quantified a total of 5317 proteins, of which 39 were connected with the protective mechanism of H2. In addition, H2 could regulate the immune and the coagulation systems. Furthermore, western blot analysis revealed that H2 decreased SAE in septic mice by downregulating the protein expression levels of SMAD4, DPYS, PTGDS and upregulating the expression level of CUL4A. These results provide insights into the mechanism of the positive effect of H2 on SAE and contribute to the clinical application of H2 in patients with sepsis.

The Effect of Thermo-Chemical Treatment on the Water Resistance of Defatted Soybean Flour-Based Wood Adhesive.

The aim of this study was to effectively improve the water resistance of a defatted soybean flour (DSF)-based adhesive by subjecting DSF to thermo-chemical treatment in the presence of sodium dodecyl sulfate (SDS), and then the crosslinking with epichlorohydrin-modified polyamide (EMPA). The effect of thermo-chemical treatment on the structures and properties of the DSF and DSF-based adhesive were investigated by plywood evaluation, boiling-water-insoluble content, and acetaldehyde value measurements, as well as FTIR, X-ray photoelectron spectroscopic (XPS), X-ray diffraction spectroscopy (XRD), thermogravimetric analysis (TGA), and rheology analyses. The test results revealed that the water resistance of the DSF-based adhesive was significantly improved, attributed to the formation of a solid three-dimensional crosslinked network structure resulted from the repolymerization of DSF, the Maillard reaction between the protein and carbohydrate, and chemical crosslinking between the crosslinker and DSF. Moreover, SDS destroyed the hydrophobic interactions within protein and inhibited macromolecular aggregations during the thermal treatment. Therefore, more reactive groups buried within the globular structure of the soybean protein component of DSF could be released, which supported the repolymerization, Maillard reaction, and chemical crosslinking of DSF, thereby leading to an improved crosslinking density of the cured DSF-based adhesive. In addition, the adhesive composed of thermo-chemically treated DSF and EMPA exhibited preferable viscosity and viscosity stability suitable for the production of wood composites.

Minocycline attenuates the development of diabetic neuropathy by inhibiting spinal cord Notch signaling in rat.

We studied the effects of minocycline (an inhibitor of microglial activation) on the expression and activity of Notch-1 receptor, and explored the therapeutic efficacy of minocycline combined with Notch inhibitor DAPT in the treatment of diabetic neuropathic pain (DNP). Diabetic rat model was established by intraperitoneal injection (ip) of Streptozotocin (STZ). Expression and activity of Notch-1 and expression of macrophage/microglia marker Iba-1 were detected by WB. Diabetes induction significantly attenuated sciatic nerve conduction velocity, and dramatically augmented the expression and the activity of Notch-1 in the lumbar enlargement of the spinal cord. Minocycline treatment, however, accelerated the decreased conduction velocity of sciatic nerve and suppressed Notch-1expression and activity in diabetic rats. Similar to DAPT treatment, minocycline administration also prolonged thermal withdrawal latency (TWL) and increase mechanical withdrawal threshold (MWT) in diabetic rats in response to heat or mechanical stimulation via inhibition the expression and the activity of Notch-1 in spinal cord. Combination of DAPT and minocycline further inhibited Notch-1 receptor signaling and reduce neuropathic pain exhibited as improved TWL and MWT. Our study revealed a novel mechanism of Notch-1 receptor inhibition in spinal cord induced by minocycline administration, and suggested that the combination of minocycline and DAPT has the potential to treat DNP.