Xue Han's research while affiliated with Sun Yat-Sen University and other places

... Indeed, nitrite has been considered a bioactive storage reservoir for NO, and reducing nitrite to NO has been considered a pharmacological strategy to restore circulating NO levels [13]. Interestingly, the nitrite reduction to NO seems to occur mainly in conditions of hypoxia, acidosis, and ischemia [14][15][16][17][18]. As demonstrated in a previous study in vitro, inorganic nitrite vasodilated human placental arteries obtained after cesarean sections following uncomplicated pregnancies [15]. ...

... The apoptotic process is similarly mediated by Caspase-3's cleavage of PARP [59]. In vivo studies have proven the cardioprotective role of anti-apoptosis during sepsis and highlighted the engagement of Bax, Bcl-2, Bcl-xl, Caspase 3, and Caspase 9 in sepsis-induced cardiomyocyte apoptosis [11,60]. In rat cardiac tissue following CLP, we noticed high expression of Cleaved-Caspase 3, Cleaved-Caspase 9, and Cleaved-PARP and low expression of Bcl-2 and Bcl-xl. ...

... Conversely, the removal of m6A is carried out by demethylases, also termed as "eraser," such as FTO and ALKBH5 [20]. Among them, FTO is an oxygen-dependent enzyme, and its activity has been reported to be severely impaired after ischemia injury in the brain, kidney, liver, heart, and other organs [30][31][32]. Notably, FTO is highly expressed in the brain, especially in neurons, and the deficiency of FTO leads to impaired learning and memory [33]. Recently, Chokkalla et al [26] demonstrated that FTO was neuronal-specific; they found that FTO was mainly expressed in neurons (NeuN+), while absent in astrocytes (GFAP+) and microglia (IBA1+) cells by immunofluorescence staining. ...

... The renal injury was observed by HE staining. According to the scoring criteria of kidney injury reported by previous literatures [28], we assessed kidney injury and presented the results in Fig. 1e. Histological scoring was done by two trained investigators in a blind fashion. ...

... The expression of PI3K and mTOR mRNA was increased by decreasing the level of miR-199a-3p. This suggests that miR-199a-3p may play a key role in the anti-apoptotic mechanism of HRS [19] . HIF-1 mediates the in ammatory response to pathogenic IIRI [20] . ...

... The result is consistent with the literature that neutrophils and monocytes/macrophages play an important role in ALI [7,8]. Therefore, neutrophils and macrophages as the main pathological cells in ALI were identified by neutrophil elastase (PMNE, which reflects neutrophils infiltration) immunohistochemistry staining and F4/80 immunofluorescence staining in lung tissue [36,37]. The increase of macrophages in the model group was reduced by 3.51 times (5.46 ± 0.82 vs 1.56 ± 0.61, P＜0.001) by XFBD-H treatment on the 2nd day and 3.37 times (3.8 ± 0.74 vs 1.13 ± 0.75，P＜0.01) on the 5th day ( Fig. 3D and E). ...

... Intriguingly, R was reported to not only stimulate S1P signaling [25] but also to inhibit S1P-producing sphingosine kinase 1 (SphK1) activity [26]. Moreover, R was shown to differentially impact human MC activation by targeting the arachidonic acid pathway and subsequent prostaglandin D2 synthesis but also by enhancing TNF release [27], whereas others reported an overall reduction in MC activation [28]. ...

... Such evidence is of great clinical relevance since ROS production, oxidative stress, and subsequent mitochondrial dysfunction are determinants during reperfusion, in causing I/R injury but may be impacted by different anesthetic agents [22]. Notably, Propofol, an intravenous anesthetic agent, chemically similar to free radical scavengers such as alpha tocopherol, has been associated with reduced damage and apoptosis in I/R injury [23,24]. Similarly, Holownia et al. [25] showed that in vitro, Propofol restored glutamine synthase activity, decreased intracellular ROS, and protected rat astrocytes from t-BOOH-induced apoptosis. ...

... A previous study found that NE is the main activity cluster of NETs [12]. Therefore, we treated the neutrophils with 44 nM sivelestat sodium, a competitive inhibitor of NE, for 30 min before and after treatment with MSU crystals [17,18], and the supernatant was co-cultured with OB. We found that adding Sivelestat sodium first rather than later could affect the osteoblasts, up-regulated the expression level of ALP and OPG, and down-regulated the expression of RANKL in osteoclast differentiation, compared with the MSU group ( Fig. 3d and e). ...

... Anesthesia/surgery increases mitochondrial permeability in hippocampal neurons, and Cyt C in the inner mitochondrial membrane is released into the cytoplasm, activating caspase-3 and caspase-7 to promote neuronal apoptosis and causing the development of PND [111,120]. A study showed that isoflurane-induced neuronal toxicity causing PND is mediated by a mitochondrial caspase-dependent apoptotic pathway in the early stages and by a caspaseindependent apoptotic pathway in the late stages [121]. c-Jun N-terminal kinase (JNK) inhibitors reverse isoflurane-induced neuronal apoptosis and long-term neurocognitive impairment by inhibiting mitochondrial intermembrane protein apoptosis-inducing factor (AIF) nuclear translocation and caspase-3 activation. ...