The free radical scavenging activity of six 2'-hydroxychalcones has been studied in gas phase and solvents using the density functional theory (DFT) method. The three main working mechanisms, hydrogen atom transfer (HAT), stepwise electron-transfer-proton-transfer (ET-PT) and sequential-proton-loss-electron-transfer (SPLET) have been considered. The O-H bond dissociation enthalpy (BDE), ionization potential (IP), proton affinity (PA) and electron transfer energy (ETE) parameters have been computed in gas phase and solvents. The theoretical results confirmed the important role of the B ring in the antioxidant properties of hydroxychalcones. In addition, the calculated results matched well with experimental values. The results suggested that HAT would be the most favorable mechanism for explaining the radical-scavenging activity of hydroxychalcone in gas phase, whereas SPLET mechanism is thermodynamically preferred pathway in aqueous solution.
Quantum-chemical computations based on the density functional theory have been employed to study the relation between the structure and the radical scavenging activity of six newly synthesized hydroxychalcones. The three main working mechanisms, hydrogen atom transfer (HAT), stepwise electron-transfer-proton-transfer, and sequential-proton-loss-electron-transfer (SPLET), were investigated, and the O-H bond dissociation enthalpy, ionization potential, proton dissociation enthalpy, and electron transfer energy parameters were computed in the gas phase and in solvents using PCM model. The geometry structure, radical, electron character, and the frontier molecular orbital were analyzed to explore the key factors that influence the radical scavenging activity of the hydroxychalcones. Results indicated that 3,4-dihydroxychalcone (6) possessing the catechol functionality is expected to be more efficient hydrogen atom and proton donor than others. The theoretical results confirm the important role of the B-ring and shed light on the role of the o-dihydroxy (catechol) moiety in the antioxidant properties of hydroxychalcones. In addition, the calculated results are in good agreement with experimental values. It was found that HAT is the most favored mechanism for explaining the radical-scavenger activity of hydroxychalcone in the gas phase, whereas SPLET mechanism is thermodynamically preferred pathway in aqueous solutions.
The overexpression of inflammasome components is correlated with diabetes‑associated complications. Oleanolic acid is a triterpenoid compound which is important in arterial injury. The present study evaluated whether oleanolic acid improved diabetic rat carotid artery injury through the inhibition of nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing‑3 (NLRP3) inflammasomes signaling pathways. A diabetic rat model was induced using streptozotocin (60 mg/kg) and underwent carotid artery injury. Morphometric analysis was performed using hematoxylin and eosin staining. The mRNA and protein levels were assayed by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. It was found that oleanolic acid (100 mg/kg/day) improved body weight, glucose metabolic disorders, neointimal hyperplasia and endothelial dysfunction in diabetic rats with carotid artery injury. In addition, oleanolic acid administration significantly downregulated the mRNA and protein expression levels of endothelin 1 in diabetic rats. Oleanolic acid decreased the intimal area and the ratio of neointima to media in diabetic rats. Serum levels of tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 in the oleanolic acid‑treated diabetic rats were downregulated. Consistent with the serum results, it was demonstrated that oleanolic acid administration caused a significant decrease in the levels of NLRP3, caspase‑1 and IL‑1β in the carotid arteries of diabetic rats. Taken together, these observations suggested that oleanolic acid attenuated carotid artery injury in diabetic rats and the underlying mechanism was mediated, at least partially, through the suppression of NLRP3 inflammasome signaling pathways.
ObjectivePineal region meningiomas are deeply located and adjacent to critical neurovascular structures, making them one of the most challenging areas to access. The authors presented a combined microscopic and endoscopic surgery and investigated its value in resecting pineal region meningiomas.MethodsTwelve patients with pineal region meningiomas from February 2017 to December 2020 were retrospectively reviewed. All patients underwent combined microscopic and endoscopic surgery using the occipital-parietal transtentorial approach. Perioperative clinical, surgical, and radiographic data were collected.ResultsThe endoscope provided a wider view and increased visualization of residual tumors. All tumors were completely resected, and none of the patients died. Total resection was believed to have been achieved in four patients, but the residual tumor was detected after endoscopic exploration and was completely resected with an endoscope. Only one patient had transient visual field deficits. No recurrence was observed during follow-up.ConclusionsCombined microscopic-endoscopic surgery for pineal region meningiomas eliminates microscopic blind spots, thus compensating for the shortcomings of the traditional occipital transtentorial approach. It is a promising technique for minimally invasive maximal resection of pineal region meningiomas.
Prostaglandin E1 (PGE1) is widely used in the treatment of limb ischemia for its potent vasodilatory and antiplatelet effects. In order to assess the curative effect of liposomal PGE1 (lipo-PGE1) as an adjuvant to surgery in patients with acute lower limb ischemia (ALLI), 204 patients who underwent hybrid procedures (operative thromboembolectomy or bypass and necessary endovascular interventions) for ALLI were randomly divided into a blank control group and a lipo-PGE1 group (intravenous infusion of 20 μg/day for 12–14 consecutive days following surgery). Patients were followed-up for 6 months after surgical revascularization for clinical events. The primary study endpoint, which was the combined incidence of perioperative (30 days) mortality (POM) and major adverse limb events (MALE; amputation or major intervention), was significantly reduced in patients treated with lipo-PGE1 (5.1% compared with 13.2% in the control group). The overall incidence of clinical events, including POM, MALE and major adverse cardiovascular events, was significantly reduced in patients receiving lipo-PGE1 (8.2%) compared with the controls (20.8%). Hybrid procedures are an improved method for treating ALLI and may remedy underlying lesions of vessels following thromboembolectomy.
Stroke is one of the leading causes of death and disability worldwide. Autophagy is a conserved cellular catabolic pathway that maintains cellular homeostasis by removal of damaged proteins and organelles, which is critical for the maintenance of energy and function homeostasis of cells. Accumulating evidence demonstrates that autophagy plays important roles in pathophysiological mechanisms under ischemic stroke. Previous investigations show that autophagy serves as a “double-edged sword” in ischemic stroke as it can either promote the survival of neuronal cells or induce cell death in special conditions. Following ischemic stroke, autophagy is activated or inhibited in several cell types in brain, including neurons, astrocytes, and microglia, as well as microvascular endothelial cells, which involves in inflammatory activation, modulation of microglial phenotypes, and blood-brain barrier permeability. However, the exact mechanisms of underlying the role of autophagy in ischemic stroke are not fully understood. This review focuses on the recent advances regarding potential molecular mechanisms of autophagy in different cell types. The focus is also on discussing the “double-edged sword” effect of autophagy in ischemic stroke and its possible underlying mechanisms. In addition, potential therapeutic strategies for ischemic stroke targeting autophagy are also reviewed.
Both primary auditory cortex (A1) and anterior auditory field (AAF) are core regions of auditory cortex of many mammalians. While the function of A1 has been well documented, the role of AAF in sound related behavioral remain largely unclear. Here in adult rats, sound cued fear conditioning paradigm, surgical ablation, and chemogenetic manipulations were used to examine the role of AAF in fear related sound context recognition. Precise surgical ablation of AAF cannot block sound cued freezing behavior but the fear conditioning became non-selective to acoustic cue. Reversible inhibition of AAF using chemogenetic activation at either training or testing phase can both lead to strong yet non-selective sound cued freezing behavior. These simple yet clear results suggested that in sound cued fear conditioning, sound cue and detailed content in the cue (e.g., frequency) are processed through distinct neural circuits and AAF is a critical part in the cortex dependent pathway. In addition, AAF is needed and playing a gating role for precise recognition of sound content in fear conditioning task through inhibiting fear to harmless cues.
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