The Recent Progress of Tricyclic Aromadendrene-Type Sesquiterpenoids: Biological Activities and Biosynthesis.

The tricyclic-aromadendrene-type sesquiterpenes are widely distributed and exhibit a range of biological activities, including anti-inflammatory, analgesic, antioxidant, antibacterial, insecticidal and cytotoxic properties. Several key sesquiterpene synthases (STSs) of this type have been identified, of which, viridiflorol synthase has been engineered for efficiently biosynthesizing viridiflorol in an strain. This paper comprehensively summarizes the distribution and biological activity of aromadendrene-type sesquiterpenes in plant essential oils and microorganisms.

Biological Properties of Sandalwood Oil and Microbial Synthesis of Its Major Sesquiterpenoids.

Sandalwood essential oil is extracted from the heartwood part of mature sandalwood and is known for its pleasant fragrance and exceptional medicinal activities, including antimicrobial, antitumor, and anti-inflammatory properties. The (Z)-α-santalol and (Z)-β-santalol are the most vital ingredients contributing to sandalwood oil's bioactivities and unique woody odor characteristics. Metabolic engineering strategies have shown promise in transforming microorganisms such as yeast and bacteria into effective cell factories for enhancing the production of vital sesquiterpenes (santalene and santalol) found in sandalwood oil.

Catalytic Mechanism and Heterologous Biosynthesis Application of Sesquiterpene Synthases.

Sesquiterpenes comprise a diverse group of natural products with a wide range of applications in cosmetics, food, medicine, agriculture, and biofuels. Heterologous biosynthesis is increasingly employed for sesquiterpene production, aiming to overcome the limitations associated with chemical synthesis and natural extraction. Sesquiterpene synthases (STSs) play a crucial role in the heterologous biosynthesis of sesquiterpene.

Two new sesquiterpenoids from plant endophytic fungus .

Two new sesquiterpenoids, flammupin A () and flammupin B (), along with two known compounds, enokipodin C () and 5,5'-dibuthoxy-2,2'-bifuran () were obtained from , an endophytic fungus isolated from the roots of Maxim. The structures were elucidated by the combination of HR-ESI-MS, NMR, and ECD analyses. Compound exhibited moderate to potent cytotoxicity against A549, HeLa, and SMMC-7721 cells with IC values ranged from 3.

Ultrahigh-Throughput Screening of High-β-Xylosidase-Producing and Investigation of the Novel β-Xylosidase Characteristics.

A droplet-based microfluidic ultrahigh-throughput screening technology has been developed for the selection of high-β-xylosidase-producing W6 from the atmospheric and room-temperature plasma-mutated library of . β-xylosidase hyperproducers filamentous fungi, W6, exhibited an increase in β-xylosidase activity by 7.1-fold.

Effects of dopamine transporter changes in the ventral tegmental area of the midbrain on cognitive function in aged rats.

The pathogenesis of Perioperative neurocognitive disorders (PND) is a synergistic effect of many factors. Up to now, the exact mechanism remains unclear. The dopamine pathway in the brain is one of the paths involved in the means of cognitive function.

Isoflurane post-conditioning contributes to anti-apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway.

The mechanisms of brain protection during ischaemic reperfusion injury induced by isoflurane (ISO) post-conditioning are unclear. Myocyte enhancement factor 2 (MEF2D) has been shown to promote neural survival in a variety of models, in which multiple survival and death signals converge on MEF2D and modulate its activity. Here, we investigated the effect of MEF2D on the neuroprotective effects of ISO post-conditioning on rats after cerebral ischaemia/reperfusion (I/R) injury.

Isoflurane Postconditioning Upregulates Phosphorylated Connexin 43 in the Middle Cerebral Artery Occlusion Model and Is Probably Associated with the TGF-1/Smad2/3 Signaling Pathway.

Aim: Connexin 43 (Cx43) has been identified to be important for cerebral ischemia/reperfusion (I/R) injury as well as protection from it. This study was aimed at investigating the relationship between phosphorylated Cx43 (p-Cx43), transforming growth factor-1 (TGF-1 (TGF.

Methods: The middle cerebral artery occlusion (MCAO) model was induced in 96 male Sprague-Dawley rats, weighing 250-300 g.

TGF-β2/Smad3 Signaling Pathway Activation Through Enhancing VEGF and CD34 Ameliorates Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats.

Evidence has shown the therapeutic potential of isoflurane (ISO) in cerebral stroke. The present study investigated the mechanism of ISO on vascular endothelial growth factor (VEGF) and CD34 expression in a rat model of stroke. Transient focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion for 24 h in rats.

TGF-β2 Induces Gli1 in a Smad3-Dependent Manner Against Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats.

Isoflurane (ISO) post-conditioning attenuates cerebral ischemia/reperfusion (I/R) injury, but the underlying mechanism is incompletely elucidated. Transforming growth factor beta (TGF-β) and hedgehog (Hh) signaling pathways govern a wide range of mechanisms in the central nervous system. We aimed to investigate the effect of the TGF-β2/Smad3 and sonic hedgehog (Shh)/Glioblastoma (Gli) signaling pathway and their crosstalk in the hippocampus of rats with ISO post-conditioning after cerebral I/R injury.

Fluoxetine mitigating late-stage cognition and neurobehavior impairment induced by cerebral ischemia reperfusion injury through inhibiting ERS-mediated neurons apoptosis in the hippocampus.

Existing evidence from clinical and animal experiments all indicated that fluoxetine, selective serotonin-reuptake inhibitor (SSRI) and anti-depressant drug, has neuroprotection and improve functional outcomes after stroke. Endoplasmic reticulum stress (ERS) inducing apoptosis after cerebral ischemia reperfusion injury was demonstrated in our previous work. This trial was examined whether fluoxetine mitigates ERS-induced neuron apoptosis.

Isoflurane Post-conditioning Ameliorates Cerebral Ischemia/Reperfusion Injury by Enhancing Angiogenesis Through Activating the Shh/Gli Signaling Pathway in Rats.

Stroke is the second leading cause of death worldwide. Angiogenesis facilitates the formation of microvascular networks and promotes recovery after stroke. The Shh/Gli signaling pathway is implicated in angiogenesis and cerebral ischemia-reperfusion (I/R) injury.

Wnt/β-catenin signaling pathway contributes to isoflurane postconditioning against cerebral ischemia-reperfusion injury and is possibly related to the transforming growth factorβ1/Smad3 signaling pathway.

Aim: The Wnt/β-catenin signaling pathway plays an important role in ischemia-reperfusion(I/R) injury, and the transforming growth factor(TGF)-β/Smad signaling pathway participates in the neuroprotection effect induced by isoflurane(ISO) postconditioning. In this study, we aimed to explore the role of the Wnt/|[beta]|-catenin β-catenin signaling pathway in the neuroprotection effect induced by ISO postconditioning, and investigate the interaction of Wnt/β-catenin and TGF-β/Smad signaling pathway in this neuroprotection effect.

Methods: Cerebral I/R injury was established in Sprague-Dawley rats by using the middle cerebral artery occlusion (MCAO) model for 90 min followed by 24 h reperfusion.

Isoflurane post-conditioning down-regulates expression of aquaporin 4 in rats with cerebral ischemia/reperfusion injury and is possibly related to bone morphogenetic protein 4/Smad1/5/8 signaling pathway.

Aim: Aquaporins (AQPs) are water-channels that play important roles in brain water homeostasis and cerebral edema induced by brain injury. This study aimed to investigate the relationship between AQP4, bone morphogenetic protein 4 (BMP4)/Smad1/5/8 signaling pathway and isoflurane post-conditiong, which has effects on brain edema in rats with cerebral ischemia/reperfusion (I/R) injury.

Methods: Cerebral I/R injury was induced in rats by using the middle cerebral artery occlusion (MCAO) model for 90min, followed by 24h of reperfusion.

Effect of ephedrine combined with bupivacaine on maternal hemodynamic and spinal nerve block in cesarean delivery.

The aim of the study was to investigate the effects of ephedrine intrathecal injection on maternal thermodynamics and spinal nerve block in cesarean section. A total of 107 patients undergoing elective cesarean section under combined spinal epidural anesthesia were randomly divided into two groups: group E: Bupivacaine (6 mg) combined with ephedrine (15 mg) and group C: Bupivacaine (6 mg). Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), the incidence of hypotension, hypertension, tachycardia, nausea and vomiting were all recorded.

Effects of activin A and its downstream ERK1/2 in oxygen and glucose deprivation after isoflurane-induced postconditioning.

Background: Isoflurane postconditioning (ISPOC) plays a neuroprotection role in the brain. Previous studies confirmed that isoflurane postconditioning can provide better protection than preconditioning in acute hypoxic-ischemic brain damage, such as acute craniocerebral trauma and ischemic stroke. Numerous studies have reported that activin A can protect rat's brain from cell injury.

Transforming growth-beta 1 contributes to isoflurane postconditioning against cerebral ischemia-reperfusion injury by regulating the c-Jun N-terminal kinase signaling pathway.

Aim: Cerebral ischemia-reperfusion (I/R) injury is a devastating complication in the perioperative period. Transforming growth factor beta (TGF-β) is a key protein that can participate in the repair and control process responses after I/R injury. Isoflurane is widely used in neurosurgery.