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1.
Sheng Wu Gong Cheng Xue Bao ; 37(8): 2765-2778, 2021 Aug 25.
Artigo em Chinês | MEDLINE | ID: mdl-34472294

RESUMO

Petroleum hydrocarbon pollutants are difficult to be degraded, and bioremediation has received increasing attention for remediating the hydrocarbon polluted area. This review started by introducing the interphase adaptation and transport process of hydrocarbon by microbes. Subsequently, the advances made in the identification of hydrocarbon-degrading strains and genes as well as elucidation of metabolic pathways and underpinning mechanisms in the biodegradation of typical petroleum hydrocarbon pollutants were summarized. The capability of wild-type hydrocarbon degrading bacteria can be enhanced through genetic engineering and metabolic engineering. With the rapid development of synthetic biology, the bioremediation of hydrocarbon polluted area can be further improved by engineering the metabolic pathways of hydrocarbon-degrading microbes, or through design and construction of synthetic microbial consortia.


Assuntos
Poluição por Petróleo , Petróleo , Poluentes do Solo , Bactérias/genética , Biodegradação Ambiental , Hidrocarbonetos , Poluição por Petróleo/análise , Microbiologia do Solo
2.
Plant Cell ; 2021 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-34469582

RESUMO

Verticillium wilt is a severe plant disease that causes massive losses in multiple crops. Increasing the plant resistance to Verticillium wilt is a critical challenge worldwide. Here, we report that the hemibiotrophic Verticillium dahliae (V. dahliae)-secreted Asp f2-like protein VDAL causes leaf wilting when applied to cotton leaves in vitro but enhances the resistance to V. dahliae when overexpressed in Arabidopsis or cotton without affecting the plant growth and development. VDAL protein interacts with Arabidopsis E3 ligases PUB25 and PUB26 (PUBs) and is ubiquitinated by PUBs in vitro. However, VDAL is not degraded by PUB25 or PUB26 in planta. Besides, the pub25 pub26 double mutant shows higher resistance to V. dahliae than the wild type. PUBs interact with the transcription factor MYB6 in a yeast two-hybrid screen. MYB6 promotes plant resistance to Verticillium wilt while PUBs ubiquitinate MYB6 and mediate its degradation. VDAL competes with MYB6 for binding to PUBs, and the role of VDAL in increasing Verticillium wilt resistance depends on MYB6. Taken together, these results suggest that plants evolute a strategy to utilize the invaded effector protein VDAL to resist the V. dahliae infection without causing a hypersensitive response (HR); alternatively, hemibiotrophic pathogens may use some effectors to keep plant cells alive during its infection in order to take nutrients from host cells. This study provides the molecular mechanism for plants increasing disease resistance when overexpressing some effector proteins without inducing HR, and may promote searching for more genes from pathogenic fungi or bacteria to engineer plant disease resistance.

3.
Aging (Albany NY) ; 12(21): 21687-21705, 2020 11 04.
Artigo em Inglês | MEDLINE | ID: mdl-33147167

RESUMO

Circular RNAs (circRNAs) have a regulatory function on inflammation and autophagy, of which rno-circRNA_010705 (circLrp1b) appears to be significantly up-regulated following traumatic brain injury (TBI). Dexmedetomidine (DEX) shows improvement effects in TBI by inhibiting NLRP3/caspase-1. However, whether circLrp1b plays critical roles in DEX-mediated TBI attenuation and the underlying mechanisms remain unclear. After TBI was established in rats by controlled cortical impact (CCI) to cause brain trauma, they received an intracerebroventricular injection of lentiviral vector, followed by intraperitoneal injection of DEX. Administration of DEX ameliorated autophagy in rats following TBI, accompanied by up-regulated circLrp1b and Dram2 and down-regulated miR-27a-3p. DEX promoted the effects of circLrp1b in attenuating TBI-induced neurologic impairment, autophagy, and inflammation, which was significantly reversed by inhibition of miR-27a-3p or Dram2 overexpression. Mechanistically, northern blot and luciferase reporter assays indicated that circLrp1b up-regulated Dram2 expression by functioning as a sponge for miR-27a-3p to promote autophagy involved in TBI, which was reversed by DEX treatment. Collectively, this study demonstrated that DEX inhibits inflammatory response and autophagy involved in TBI in vivo through inactivation of the circLrp1b/miR-27a-3p/Dram2 signaling pathway.


Assuntos
Anti-Inflamatórios/farmacologia , Autofagia/efeitos dos fármacos , Lesões Encefálicas Traumáticas/tratamento farmacológico , Encéfalo/efeitos dos fármacos , Dexmedetomidina/farmacologia , Mediadores da Inflamação/metabolismo , MicroRNAs/metabolismo , RNA Circular/metabolismo , Animais , Comportamento Animal/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Encéfalo/fisiopatologia , Lesões Encefálicas Traumáticas/metabolismo , Lesões Encefálicas Traumáticas/patologia , Lesões Encefálicas Traumáticas/fisiopatologia , Modelos Animais de Doenças , Regulação da Expressão Gênica , Masculino , MicroRNAs/genética , RNA Circular/genética , Ratos Sprague-Dawley , Transdução de Sinais
4.
Neurotox Res ; 38(2): 299-311, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32458405

RESUMO

Recent pre-clinical and clinical studies suggest that general anesthesia in infants and children may increase the risk of learning disabilities. Currently, there is no treatment for preventing anesthesia-induced neurotoxicity and potential long-term functional impairment. Animal studies have shown that neonatal exposure to anesthesia can induce acute neurotoxicity and long-term behavioral changes that can be detected a few months later. It is currently unknown whether neonatal exposure, especially repeated exposures, to general anesthesia can induce or increase the risk for cognitive impairment during aging. Here, we report that repeated exposures of neonatal mice (P7-9 days old) to anesthesia with sevoflurane (3 h/day for 3 days) led to cognitive impairment that was detectable at the age of 18-19 months, as assessed by using novel object recognition, Morris water maze, and fear conditioning tests. The repeated neonatal exposures to anesthesia did not result in detectable alterations in neurobehavioral development, in tau phosphorylation, or in the levels of synaptic proteins in the aged mouse brains. Importantly, we found that treatment with intranasal insulin prior to anesthesia exposure can prevent mice from anesthesia-induced cognitive impairment. These results suggest that neonatal exposure to general anesthesia could increase the risk for cognitive impairment during aging. This study also supports pre-treatment with intranasal administration of insulin to be a simple, effective approach to prevent infants and children from the increased risk for age-related cognitive impairment induced by neonatal exposure to general anesthesia.


Assuntos
Anestésicos Inalatórios/toxicidade , Cognição/efeitos dos fármacos , Hipoglicemiantes/farmacologia , Insulina/farmacologia , Sevoflurano/toxicidade , Administração Intranasal , Anestesia Geral/efeitos adversos , Animais , Animais Recém-Nascidos , Comportamento Animal/efeitos dos fármacos , Disfunção Cognitiva , Condicionamento Psicológico/efeitos dos fármacos , Camundongos , Teste do Labirinto Aquático de Morris/efeitos dos fármacos , Teste de Campo Aberto/efeitos dos fármacos , Pré-Medicação , Proteínas tau/efeitos dos fármacos , Proteínas tau/metabolismo
5.
PLoS One ; 15(4): e0231090, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32240260

RESUMO

Sevoflurane and isoflurane are among the most commonly used general anesthetics for children including infants, but their impact on metabolism, especially on blood glucose level, in children is not well understood. We investigated the impacts of anesthesia of neonatal (7-8 days old) and adult (2-3 months old) mice with the inhalational anesthetics 2.5% sevoflurane or 1.5% isoflurane, or the injectable anesthetics propofol (150 mg/kg) or avertin (375 mg/kg), for up to 6 hours. We found that sevoflurane and isoflurane induced severe hypoglycemia in neonatal mice and that this phenomenon was specific to the inhalational anesthetics because the injectable anesthetics propofol and avertin did not induce hypoglycemia. Surprisingly, the inhalational anesthesia induced hyperglycemia instead in adult mice. We also demonstrated that the inhalational anesthesia-induced hypoglycemia was a major cause of death for the neonatal mice receiving intranasal administration of saline prior to anesthesia. These studies revealed severe hypoglycemia in neonatal mice during anesthesia with sevoflurane or isoflurane. If this phenomenon also occurs in human, our findings would warrant closely monitoring blood glucose level and maintaining it in the normal range in infants receiving inhalational anesthesia.


Assuntos
Hipoglicemia/induzido quimicamente , Isoflurano/efeitos adversos , Sevoflurano/efeitos adversos , Período de Recuperação da Anestesia , Anestesia por Inalação , Anestésicos Inalatórios/efeitos adversos , Anestésicos Intravenosos/efeitos adversos , Animais , Animais Recém-Nascidos , Glicemia/metabolismo , Etanol/análogos & derivados , Etanol/farmacologia , Hipoglicemia/sangue , Insulina/sangue , Camundongos Endogâmicos C57BL , Propofol/farmacologia
6.
Front Neurosci ; 13: 706, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31354415

RESUMO

Children, after multiple exposures to general anesthesia, appear to be at an increased risk of developing learning disabilities. Almost all general anesthetics-including sevoflurane, which is commonly used for children-are potentially neurotoxic to the developing brain. Anesthesia exposure during development might also be associated with behavioral deficiencies later in life. To date, there is no treatment to prevent anesthesia-induced neurotoxicity and behavioral changes. In this study, we anesthetized 7-day-old neonatal mice with sevoflurane for 3 h per day for three consecutive days and found that the anesthesia led to mild behavioral abnormalities later in life that were detectable by using the novel object recognition test, Morris water maze, and fear conditioning test. Biochemical and immunohistochemical studies indicate that anesthesia induced a decrease in brain levels of postsynaptic density 95 (PSD95), a postsynaptic marker, and marked activation of neuronal apoptosis in neonatal mice. Importantly, insulin administered through intranasal delivery prior to anesthesia was found to prevent the anesthesia-induced long-term behavioral abnormalities, reduction of PSD95, and activation of neuronal apoptosis. These findings suggest that intranasal insulin administration could be an effective approach to prevent the increased risk of neurotoxicity and chronic damage caused by anesthesia in the developing brain.

7.
Biosci Rep ; 38(5)2018 10 31.
Artigo em Inglês | MEDLINE | ID: mdl-30232232

RESUMO

The abnormally high nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activity is a typical characteristic of traumatic brain injury (TBI). Dexmedetomidine (Dex) is a highly selective α-2 adrenergic receptor agonist that inhibits the activation of NLRP3. Thus, it was hypothesized that Dex could attenuate TBI by inhibiting NLRP3 inflammasome activity in hippocampus. Rats were subjected to controlled cortical impact method to induce TBI, and treated with Dex. The effect of Dex treatment on the cognitive function, NLRP3 activity, and microglial activation in rat brain tissues was assessed. The administration of Dex improved performance of TBI rats in Morris water maze (MWM) test, which was associated with the increased neurone viability and suppressed microglia activity. Moreover, the administration of Dex inhibited the neuroinflammation in brain tissue as well as the expressions of NLRP3 and caspase-1. Additionally, Dex and NLRP3 inhibitor, BAY-11-7082 had a synergistic effect in inhibiting NLRP3/caspase-1 axis activity and improving TBI. The findings outlined in the current study indicated that the improvement effect of Dex on TBI was related to its effect on NLRP3 activity.


Assuntos
Lesões Encefálicas Traumáticas/tratamento farmacológico , Dexmedetomidina/administração & dosagem , Inflamassomos/efeitos dos fármacos , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Animais , Lesões Encefálicas Traumáticas/genética , Lesões Encefálicas Traumáticas/patologia , Caspase 1/genética , Modelos Animais de Doenças , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Humanos , Inflamassomos/metabolismo , Microglia/efeitos dos fármacos , Microglia/patologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/antagonistas & inibidores , Neurônios/efeitos dos fármacos , Neurônios/patologia , Ratos
8.
Bioprocess Biosyst Eng ; 41(1): 135-141, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29018957

RESUMO

Ganoderma lucidum is a traditional Chinese medicine, and its polysaccharides possess diverse and significant pharmacological activities. This study aimed to investigate the polysaccharide production, molecular characteristics and in-vitro antioxidant activity of G. lucidum fruiting body after the mushroom was harvested and treated with heat stress (HS). HS enhanced the production of polysaccharides after harvest and treatment of 42 °C HS for 2 h, and that resulted in the highest polysaccharide yield of 10.50%, which was 45.63% higher than that of the control, while 37, 45 °C HS had no significant effect on the production. In terms of molecular characteristics, 42 °C HS significantly changed monosaccharide ratio of polysaccharides, but no apparent molecular weight and functional group changes were found in polysaccharides after HS treatment. The results of in-vitro antioxidant activity assay revealed that 42 °C HS significantly improved the antioxidant activities of polysaccharides at the concentration of 2 mg/mL. In conclusion, this study provides a promising strategy to improve the production of G. lucidum fruiting body polysaccharides.


Assuntos
Antioxidantes/metabolismo , Carpóforos/metabolismo , Polissacarídeos Fúngicos/biossíntese , Resposta ao Choque Térmico/fisiologia , Reishi/metabolismo
9.
Neurochem Res ; 41(9): 2425-32, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27233246

RESUMO

Bupivacaine is widely used for regional anesthesia, spinal anesthesia, and pain management. However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In the present study, we tested whether curcumin could attenuate bupivacaine-induced neurotoxicity in SH-SY5Y cells. Cell injury was evaluated by examining cell viability, mitochondrial damage and apoptosis. We also investigated the levels of activation of the Akt signaling pathway and the effect of Akt inhibition by triciribine on cell injury following bupivacaine and curcumin treatment. Our findings showed that the bupivacaine treatment could induce neurotoxicity. Pretreatment of the SH-SY5Y cells with curcumin significantly attenuated bupivacaine-induced neurotoxicity. Interestingly, the curcumin treatment increased the levels of Akt phosphorylation. More significantly, the pharmacological inhibition of Akt abolished the cytoprotective effect of curcumin against bupivacaine-induced cell injury. Our data suggest that pretreating SH-SY5Y cells with curcumin provides a protective effect on bupivacaine-induced neuronal injury via activation of the Akt signaling pathway.


Assuntos
Bupivacaína/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Curcumina/farmacologia , Neurônios/efeitos dos fármacos , Síndromes Neurotóxicas/tratamento farmacológico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Neurônios/metabolismo , Fármacos Neuroprotetores/farmacologia , Síndromes Neurotóxicas/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Fosforilação/efeitos dos fármacos
10.
Gynecol Endocrinol ; 32(7): 581-6, 2016 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-26878683

RESUMO

Atherosclerosis is an inflammatory disease and involves migration of vascular smooth muscle cells (VSMCs). Estrogen inhibits VSMCs migration, while the underlying mechanism remains to be revealed. Recent years, there is emerging evidence showing that TNF-related apoptosis-inducing ligand (TRAIL) increases proliferation and migration of VSMCs. In this study, we investigated the regulatory effect of estrogen on TRAIL expression in VSMCs. TNF-α greatly enhanced TRAIL protein expression and stimulated VSMCs proliferation and migration. This effect was partially inhibited by the addition of TRAIL neutralizing antibody, suggesting that TRAIL is important in TNF-α-induced migration. 17ß-estradiol (E2) inhibited TRAIL expression under TNF-α stimulation in a time- and concentration-dependent manner. This effect was was mimicked by ERα agonist 4',4″,4‴-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT), but not ERß agonist 2,3-bis-(4-hydroxyphenyl)-propionitrile (DPN), indicating that ERα is involved in this action. TNF-α led to nuclear factor kappa B (NF-κB) p65 phosphorylation and the inhibitor pyrrolidine dithiocarbama (PDTC) inhibited TRAIL expression, suggesting that NF-κB signaling is crucial for TARIL production. E2 suppressed p65 phosphorylation in VSMCs and the overexpression of p65 subunit reversed the inhibitory effect of E2 on TRAIL expression and cell proliferation and migration. Taken together, our results indicate that E2 inhibits VSMCs proliferation and migration by downregulation of TRAIL expression via suppression of NF-κB pathway.


Assuntos
Movimento Celular/fisiologia , Proliferação de Células/fisiologia , Estradiol/metabolismo , Músculo Liso Vascular/efeitos dos fármacos , Miócitos de Músculo Liso/efeitos dos fármacos , NF-kappa B/metabolismo , Ligante Indutor de Apoptose Relacionado a TNF/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Animais , Células Cultivadas
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