Cell Differentiation ; Nicotine/pharmacology* ; Osteogenesis/physiology* ; Periodontal Ligament ; Stem Cells

Nicotine enhances the function of learning and memory, but the underlying mechanism still remains unclear. Hippocampal long-term potentiation (LTP) is assumed to be a cellular mechanism of learning and memory. Our previous experiments showed that with the single pulses evoking 80% of the maximal population spike (PS) amplitude, nicotine (10 μmol/L) induced LTP-like response in the hippocampal CA1 region. In the present study, the nicotinic acetylcholine receptor (nAChR) subtypes and relevant neurotransmitter releases involved in LTP-like response induced by nicotine were investigated by extracellularly recording the PS in the pyramidal cell layer in the hippocampal CA1 region in vitro. LTP-like response induced by nicotine was blocked by mecamylamine (1 μmol/L) or κ-bungarotoxin (0.1 μmol/L), but not by dihydro-β-erythtroidine (DHβE, 10 μmol/L). Moreover, it was inhibited by propranolol (10 μmol/L), but not by phentolamine (10 μmol/L) or atropine (10 μmol/L). The results suggest that noradrenaline release secondary to the activation of κ-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CA1 region.
Animals ; Bungarotoxins ; CA1 Region, Hippocampal ; physiology ; Long-Term Potentiation ; drug effects ; Nicotine ; pharmacology ; Norepinephrine ; secretion ; Receptors, Nicotinic ; metabolism

Blakeslea trispora is a natural source of carotenoids, including β-carotene and lycopene, which have industrial applications. Therefore, classical selective breeding techniques have been applied to generate strains with increased productivity, and microencapsulated β-carotene preparation has been used in food industry (Li et al., 2019). In B. trispora, lycopene is synthesized via the mevalonate pathway (Venkateshwaran et al., 2015). Lycopene cyclase, which is one of the key enzymes in this pathway, is a bifunctional enzyme that can catalyze the cyclization of lycopene to produce β-carotene and exhibit phytoene synthase activity (He et al., 2017).
Citric Acid Cycle ; Fermentation ; Gas Chromatography-Mass Spectrometry/methods* ; Lycopene/metabolism* ; Mucorales/metabolism* ; Nicotine/pharmacology* ; beta Carotene/biosynthesis*

OBJECTIVETo explore the effect of nicotine on the autophagy level of human periodontal ligament cells (hPDLCs).

METHODSPeriodontal tissues collected from premolars for orthodontic treatment reasons were used to culture hPDLCs. Western blot analysis was performed to test the most optimal time and concentration of nicotine on the autophagy level of the hPDLCs. Transmission electron microscope and immunofluorescence observation were carried out to detect the form of autophagosomes and expression of autophagy related protein LC3 in hPDLCs under this optimal condition.

RESULTSProtein expression of LC3Ⅱ was up regulated with the 12 h nicotine stimulating. Besides that, the up regulation of the protein expression of LC3Ⅱ was concentration dependent and nicotine with a concentration of 1×10⁻⁵ mol·L⁻¹ was the most optimal condition. Transmission electron microscope and immunofluorescence observations indicated that nicotine would activate the autophagy level of hPDLCs by increasing the number of autophagosomes and up regulating the expression of autophagy related protein LC3.

CONCLUSIONSNicotine could increase autophagy level of hPDLCs, thus affecting the occurrence and development of smoking related periodontitis.

Autophagy ; Blotting, Western ; Cell Culture Techniques ; Cells, Cultured ; Humans ; Microtubule-Associated Proteins ; Nicotine ; pharmacology ; Nicotinic Agonists ; pharmacology ; Periodontal Ligament ; Periodontitis ; Up-Regulation

A novel series of bis-nicotine derivatives (3a-3i) were designed, synthesized and evaluated as bivalent anti-Alzheimer's disease agents. The pharmacological results indicated that compounds 3e-3i inhibited both acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in the micromolar range (IC50, 2.28-117.86 micromol x L(-1) for AChE and 1.67-125 micromol x L(-1) for BChE), which was at the same potency as rivastigmine. A Lineweaver-Burk plot and molecular modeling study showed that these derivatives targeted both the catalytic active site (CAS) and the peripheral anionic site (PAS) of AChE. Besides, these compounds could significantly inhibit the self-induced Abeta aggregation with inhibition activity (11.85%-62.14%) at the concentration of 20 micromol x L(-1).
Acetylcholinesterase ; metabolism ; Amyloid beta-Peptides ; antagonists & inhibitors ; metabolism ; Binding Sites ; Butyrylcholinesterase ; metabolism ; Cholinesterase Inhibitors ; chemical synthesis ; chemistry ; pharmacology ; Nicotine ; analogs & derivatives ; chemical synthesis ; chemistry ; pharmacology

AIMTo observe the effect of angiotensin-converting enzyme inhibitors (ACEI) and aldosterone receptor blockers on cardiac function to explore the mechanism of cardiac function descending and myocardial injury in calcium-overload rats.

METHODSCalcium-overload in rat was induced by administration of Vitamin D3 plus nicotine. To Estimate the extent of calcium-overload by calcium content. Angiotension II and aldosterone levels in the myocardia were measured by radioimmunoassay. Cardiac function (+/- LVdp/dt, LVESP and LVEDP) were measured by Powerlab. The malondialdehyde (MDA) content, activities of lactate dehydrogenase (LDH) and creatine kinase (CPK) were measured by biochemistry.

RESULTSCalcium content increased by 3.2-, 5.8 -fold in myocardial and artery, compared with controls. VDN-treated survivors showed lower + LVdp/dt(max) and -LVdp/dt(max) values, by 27% and 34%, respectively (both P < 0.01). Higher LVESP, and LVEDP by 42 % and 32% (P < 0.01); heart rate and mean arterial pressure were not significantly altered (P > 0.05). The lipid peroxidation products MDA and conjugated diene in myocardia were increased 22% (P < 0.01), 68% (P < 0.05) (P < 0.05), respectively. The plasma activity of CPK and LDH was greatly increased by 4.5-and 3.1-fold (P < 0.01), respectively. ACEI and spironolactone obviously relieved degree of calcium-overload and improved cardiac function and myocardial injury(P < 0.01). Calcium content in myocardia and artery was lower 44%, 39% and 57%, 34%. Lower MDA by 20%, 30%, lower conjugated diene by 44%, 35% than calcium-overload group. The plasma activity of CPK and LDH were obviously decreased 28%, 34% and 20%, 27%, compared with calcium-overload group.

CONCLUSIONCalcium-overload could lead to cardiac function descending and myocardial injury in calcium-overload rats by VDN. ACEI and spironolactone could reduce calcium-overload in myocardial and ameliorate cardiac function and decrease myocardial injury.

Angiotensin-Converting Enzyme Inhibitors ; pharmacology ; Animals ; Calcium ; adverse effects ; Creatine Kinase ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lipid Peroxidation ; Male ; Malondialdehyde ; analysis ; Mineralocorticoid Receptor Antagonists ; Myocardium ; metabolism ; Nicotine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Spironolactone ; pharmacology ; Vitamin D ; pharmacology

OBJECTIVETo investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro.

METHODMouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured.

RESULTSCSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 mumol/L Ca2+, but promoted swelling response at 250 mumol/L Ca2+. Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved.

CONCLUSIONThe toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.

Adenosine Triphosphatases ; pharmacology ; Animals ; Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Brain ; pathology ; Electron Transport Complex IV ; pharmacology ; Free Radicals ; Ganglionic Stimulants ; toxicity ; Mice ; Mitochondria ; pathology ; Nicotine ; toxicity ; Smoke ; adverse effects ; Tobacco

OBJECTIVETo investigate the effects of arecoline and nicotine on the expression of human telomerase reverse transcriptase (hTERT) mRNA and protein in cultured normal human oral keratinocytes (KC).

METHODSThe experiments were divided into arecoline group, arecoline/nicotine group and control group. The hTERT mRNA and protein expression of KC was examined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot.

RESULTSArecoline could induce the hTERT mRNA and protein expression of KC in a dose dependent manner, the hTERT mRNA and protein expression of KC was higher in 0.030, 0.060, 0.090 g/L arecoline group than control group (P < 0.001). Nicotine (0.025 g/L) increased hTERT mRNA and protein expression of KC induced by arecoline.

CONCLUSIONSArecoline could increase the expression of hTERT mRNA and protein in oral keratinocytes. Nicotine had a synergistic effect on arecoline. hTERT over-expression induced by arecoline and nicotine may play an important role in the malignant transformation of oral submucous fibrosis.

Arecoline ; pharmacology ; Cells, Cultured ; Cholinergic Agonists ; pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Ganglionic Stimulants ; pharmacology ; Humans ; Keratinocytes ; drug effects ; enzymology ; Mouth Mucosa ; enzymology ; pathology ; Nicotine ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Telomerase ; genetics ; metabolism

OBJECTIVETo examine the expression and subcellular localization of transcription factor USF1 in odontoblasts and investigate whether nuclear translocation occurs under stimuli.

METHODSOdontoblasts MDPC-23 were cultured on coverslips and divided into 2 groups. Group 1 received no stimuli, and group 2 was stimulated by nicotine with various concentrations respectively for 1h. Then the mountings of odontoblasts were prepared and immunocytochemical staining was performed with specific USF1 antibody via SABC method. Hela cells were used as positive control.

RESULTSThe staining was positive in the cytoplasm of odontoblasts in group 1, but in the nuclei of Hela cells and in 100 mg/L nicotine-stimulated odontoblasts in group 2.

CONCLUSIONSThere exists USF1 protein in odontoblasts, which locates in the cytoplasm and could translocate into nuclei under the stimulation of nicotine.

Cells, Cultured ; HeLa Cells ; Humans ; Nicotine ; pharmacology ; Odontoblasts ; drug effects ; metabolism ; Protein Sorting Signals ; Protein Transport ; drug effects ; Upstream Stimulatory Factors ; metabolism

OBJECTIVETo review the current evidence that links smoking to obstructive sleep apnea (OSA) and to discuss some potential mechanisms proposed for these links.

DATA SOURCESWe searched PubMed and Medline to identify studies investigating the interaction between smoking and OSA.

STUDY SELECTIONArticles regarding the relationship between smoking and OSA were selected. Studies considered smoking as a confounding factor were excluded.

RESULTSThe association of smoking and OSA has been confirmed in several studies. The effects of smoking on the pathophysiology of OSA may include smoking-induced upper airway inflammation, stimulant effects of nicotine on upper airway muscles, and a "rebound effect" due to nightly short-term nicotine withdrawal, or all of the above. In addition, the coexistence of OSA and smoking may have more widespread implications for cardiovascular dysfunction in patients with OSA. Finally, OSA might be responsible for the addiction to nicotine.

CONCLUSIONSSmoking may act as a risk factor for OSA and join with OSA in a common pathway to increase the risk of systematic injury. OSA, in turn, may be a predisposing factor for smoking. Thus, smoking cessation is recommended when considering treatment for OSA, and treating OSA may be a necessary precondition for successful smoking cessation.

Asthma ; epidemiology ; etiology ; Bronchi ; drug effects ; Humans ; Nicotine ; pharmacology ; Risk Factors ; Sleep ; physiology ; Sleep Apnea, Obstructive ; epidemiology ; etiology ; Smoking ; adverse effects ; Tobacco Use Disorder ; epidemiology ; etiology