Pantranscriptome combined with phenotypic quantification reveals germplasm kinship and regulation network of bract color variation in Bougainvillea.

Bracts are the metamorphic non-flower organ in angiosperm plants. The variation of the color and shape of bracts was found to be neo-functionalized (i.e., similar to petals), garnering research interest as a pollinator attractor. Bougainvillea is known for its specialized, large, and colorful bracts, which contrast with its tiny colorless flowers. As a plant whose bracts vary greatly in terms of coloration, the molecular mechanisms for Bougainvillea bract coloration and polychroism are largely unknown. The lack of genomic information for Bougainvillea largely hinders studies into the evolution and genetic basis of bract color variation. In this study, a pan-transcriptome of bracts obtained from 18 Bougainvillea glabra accessions was employed to investigate the global population-level germplasm kinship and the gene regulation network for bract color variation. Our results showed that the bracts of B. glabra accessions have largely differentiated International Commission on Illumination (CIE) L-a-b values. Moreover, germplasm kinship detected using principal component analysis, phylogeny, and admixture analysis showed three optimal subgroups, two of them distinctly clustered, which were not directly correlated with bract color variation at the population level. Differentially expressed genes (DEGs) between accessions of high vs. low L-a-b values revealed several considerable upregulated genes related to bract color L-a-b variation. A weighted gene co-expression network was constructed, and eight co-expressed regulation modules were identified that were highly correlated with variation in bract CIE L-a-b color values. Several candidate DEGs and co-expressed hub genes (e.g., GERD, SGR, ABCA3, GST, CYP76AD1, CYP76C, and JAZ) that were tightly associated with bract color variation were eventually determined responsible for L-a-b colorations, which might be the core regulation factors contributing to the B. glabra bract color variation. This study provides valuable insights into the research on germplasm kinship, population-level pan-transcriptome expression profiles, and the molecular basis of color variation of key innovative bracts in horticultural Bougainvillea.

Effect of Thiopental on Ischemic Stroke in Rat Brain in Spontaneously Hypertensive Rats.

Motivation and Problem Statement. Thiopental is an anesthetic drug related to the condition of controlling the area of neurological contexts. This study is related to the analysis of effectiveness for the condition of thiopental application on spontaneously hypertensive rats. Methodology. We have evaluated the thiopental induction as the anesthetic agent. The hypertensive rats were selected to administer thiopental in the form of anesthesia. The selection and application of hypertensive strokes are related to the derivation of an inducible model to assess the efficacy for analyzing the ischemic stroke parameters which relate to the human body. We used middle cerebral artery occlusion (MCAO) models related to spontaneous hypertension with the area of examining the complications in ischemic stroke. Results and Conclusion. The study focused on the experimental analysis based on the selection of spontaneously hypertensive rats associated with the incidence of ischemic stroke. Application of thiopental has reported the weak functionality and mechanism on the relaxation of neuronal activity in the case of rat brain. The considered population of the spontaneously hypertensive rats is evaluated based on the condition of effectiveness as well as the duration of the medication effects within the rat brain. Involvement of thiopental in the case of ischemic stroke has provided the area of risk development for high rate of death incidences after occurrence of acute ischemic stroke. A complication in the area of defining neuroprotective actions provides difficulty in drawing an appropriate conclusion of the study.

Molecular Mechanism of Gas Anesthetics on the Invasion, Metastasis, and Chemosensitivity of Osteosarcoma Cells.

BACKGROUND: Osteosarcoma is one of the most prominent bone cancers which has a predominant occurrence in children and adolescents. This study is focused on determining the effects of treatment of gas anesthetics on invasion, metastasis, and chemosensitivity in the progression of osteosarcoma cells. Material and Methods. The biological effects of the common gas anesthetics-desflurane, isoflurane, and sevoflurane-on osteosarcoma cells were studied and compared. The biological assays were performed for analysis of cell migration and proliferation. RESULTS: Isoflurane and sevoflurane have shown significant inhibition in the osteosarcoma cells at clinically relevant concentrations. Desflurane has shown less potent action on cell migration and inhibition. All three gas anesthetics have shown inhibition in cell proliferation. The effective antiproliferative action was at a clinically significant dose. At low millimolar concentrations, cell apoptosis was moderately affected. Drug combination analysis with chemotherapeutic drugs showed relevant inhibition in cell migration. All three agents showed significant augmentation of chemotherapeutic drugs in suppression and inhibition of inducing apoptosis. The antimigration action is likely to affect the PI3K/AKT pathway and IGF-1. CONCLUSION: The study demonstrates the proposed mechanisms of gas anesthetics and their differential effects on osteosarcoma cells and their survival, migration, growth, and chemosensitivity.

Propofol Alleviates Neuropathic Pain Induced by Chronic Contractile Injury by Regulating the Spinal glun2b-p38mapkepac1 Pathway.

BACKGROUND: Propofol acts as an intravenous anesthetic cure which is widely used as a therapy for the craniocerebral injury that comprised surgical anesthesia as well as the sedation done in the intensive care units. Propofol is one of the most commonly used and efficient anesthetics where the painful effects are followed by an injection of propofol. In many cases, patients experience pain followed by anxiety, boredom, fear, and even myocardial ischemia. OBJECTIVE: This study was performed to investigate the underlying mechanism of propofol and its effect on regulating spinal glun2b-p38mapkepac1 pathways in chronic contractile injury. Material and Methods. Contractile injury was performed by ligation around the nerve of the thigh region postanesthesia. Rats were divided into three groups to analyze the changes like mechanical allodynia by the paw withdrawal threshold and histopathological analysis for assessing cellular degradation. L4-L6 from the spinal dorsal horns were isolated and harvested for studying protein expression, by the method of western blotting and immunofluorescence analysis. RESULTS: The pain caused due to mechanical allodynia in the paw region was highest at 1 hour postinduction and lasted for three days postinjury. Pain was significantly less in the group receiving propofol when compared with the isoflurane group for the first two hours of injury. In the propofol group, EPAC1, GluN2B, and p38 MAP K were significantly lower. CONCLUSION: In the rat model of induced chronic contractile injury, postsurgery there was a suppression of the GluN2B-p38MAPK/EPAC1 signaling pathway in the propofol group. As the p38MAPK/EPAC pathway has a significant role in the postoperative hyperalgesia, thus our experiment suggests that propofol has analgesic effects.

Dexmedetomidine-up-regulated microRNA-381 exerts anti-inflammatory effects in rats with cerebral ischaemic injury via the transcriptional factor IRF4.

Dexmedetomidine (Dex) possesses analgesic and anaesthetic values and reported being used in cerebral ischaemic injury therapeutics. Accumulating studies have determined the effect of microRNAs (miRNAs) on the cerebral ischaemic injury. Thus, the present study aimed to unravel the molecular mechanism of miR-381 and Dex in cerebral ischaemic injury. For this purpose, the cerebral ischaemic injury rat model was established by induction of middle cerebral artery occlusion (MCAO) and expression of miR-381 and IRF4 was determined. Thereafter, MCAO rats were treated with Dex, miR-381 mimic, miR-381 inhibitor and oe-IRF4 respectively, followed by evaluation of neurological function. Furthermore, neuron cells were isolated from the hippocampus of rats and subjected to oxygen-glucose deprivation (OGD). Then, OGD-treated neuron cells and primary neuron cells were examined by gain- and loss-of-function assay. Neuron cell apoptosis was detected using TUNEL staining and flow cytometry. The correlation between interferon regulatory factor 4 (IRF4) and interleukin (IL)-9 was detected. Our results showed down-regulated miR-38 and up-regulated IRF4 in MCAO rats. Besides, IRF4 was targeted by miR-381 in neuron cells. Dex and overexpressed miR-381, or silenced IRF4 improved the neurological function and inhibited neuron cell apoptosis in MCAO rats. Additionally, in MCAO rats, Dex was found to increase the miR-381 expression and reduced IRF4 expression to decrease the IL-9 expression, which suppressed the inflammatory response and cell apoptosis both in vivo and in vitro. Importantly, our study demonstrated that Dex elevated the expression of miR-381, which ultimately results in the inhibition of inflammation response in rats with cerebral ischaemic injury.

Long non-coding RNA MALAT1 sponges microRNA-429 to regulate apoptosis of hippocampal neurons in hypoxic-ischemic brain damage by regulating WNT1.

Hypoxic-ischemic brain damage (HIBD) is a common neurological disorder. Emerging reports reveal that long non-coding RNAs and microRNAs (miRs) are implicated in the progress of HIBD. In this study we tried to ascertain whether lncRNA MALAT1, with the involvement of miR-429 and WNT1, affects HIBD. Initially, a HIBD mouse model was established. Then, we treated HIBD mice with dexmedetomidine (DEX) and then up- or down-regulated the expression of MALAT1, miR-429 and WNT1 in HIBD mice and neurons. Meanwhile, brain injury and hippocampal neuronal apoptosis were evaluated. Moreover, the interaction among MALAT1, miR-429 and WNT1 in HIBD was investigated. MALAT1 and WNT1 were high-expressed in brain tissues of HIBD mice while miR-429 was low-expressed in brain tissues from HIBD mice. Interestingly, MALAT1 silencing was observed to enhance the cerebral protection of DEX against HIBD. In addition, it was confirmed that MALAT1 sponged miR-429 downregulating expression of miR-429, thereby promoting apoptosis of hippocampal neurons. This effect was achieved through up-regulating the level of WNT1. Taken together, this study demonstrates that silencing of MALAT1 enhances the cerebral protection of DEX against HIBD by suppressing WNT1 expression through miR-429.