• Biomolecules & Therapeutics
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• v.4 no.2
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• pp.167-173
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• 1996

This study was undertaken to evaluate a behavior-electroencephalogram (EEG) pattern relationship in pilocarpine- and kainic acid-induced convulsions of rats. Also we intended to examine the effect of a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801, and diazepam on the pilocarpine-induced behavioral and electrical seizures in rats. The electrical activities at frontal and hippocampal areas and behavior activities were measured in freely moving rats. At the beginning of the experiments, the rats displayed an exploratory behavior. This awake and moving phase with a low amplitude, irregular, 4-10 Hz wave was followed by a still phase. Pilocarpine (400 mg/kg, i.p.) and kainic acid (0.5 mg/kg, i.c.v.) induced tonic and clonic seizures. The pilocarpine-induced change in electrical activities exhibited a weak correlation with behavioral convulsion at all stages. The amplitude and duration of the electrical response were not linear with the degree of behavioral score. An application of MK-801 (dizocilpine, 7.5 mg/kg) did not affect the amplitudes of the convulsant-induced electrical activities, though the same dose of this drug caused the deformation of the electrical pattern. There was no effect of MK-801 on the behavioral and electrical activities as expected. Diazepam (1 mg/kg) did not affect the amplitude of the electrical activities induced by pilocarpine but changed the pattern of these activities. Our study shows that there is no linear relationship between degree of behavior and amplitude of electrical activities of convulsants. This may indicate that the NMDA receptor stimulation can be processed by the neocortical or hippocampal network in a different way between behavioral and electrical activities.

• Journal of Oral Medicine and Pain
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• v.24 no.4
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• pp.347-359
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• 1999

The purpose of this study was to investigate the effect of pilocarpine containing chewing gum on anti-microbial components in whole saliva of xerostomic patients, The objective xerostomic patients were instructed to use 5mg-pilocarpine containing chewing gum for 20minutes three times per day, and the author measured the flow rates of unstimulated whole saliva and stimulated whole saliva at the beginning the treatment, 1,2,3, and 4 weeks after. The concentration and flow rate of anti-microbial components in whole saliva were quantitated by enzyme-linked immunosorbent assay(ELISA). The obtained results were as follows: 1. There were significant increase in the unstimulated and stimulated whole salivary flow rate after using pilocarpine-containing chewing gum in xerostomic patients. 2. The concentrations of IgA in the unstimulated and stimulated whole saliva showed increasing pattern but, no significant changes, arid the flow rates of IgA in the unstimulated and stimulated whole saliva showed significant increase after using pilocarpine-containing chewing gum in xerostomic patients. 3. The concentrations of IgM in the unstimulated and stimulated whole saliva showed increasing pattern but, no significant changes, and the flow rates of IgM in the unstimulated and stimulated whole saliva showed significant increase after using pilocarpine-containing chewing gum in xerostomic patients. 4. The concentrations of lactoferrin in the unstimulated and stimulated whole saliva showed no significant changes, and the flow rates of lactoferrin in the unstimulated and stimulated whole saliva showed significant increase after using pilocarpine-containing chewing gum in xerostomic patients. 5. The concentrations of lysozyme in the unstimulated and stimulated whole saliva showed no significant changes, and the flow rates of lysozyme in the unstimulated whole saliva showed significant increase, but in stimulated whole saliva showed no significant changes after using pilocarpine-containing chewing gum in xerostomic patients.

• Journal of Korean Academy of Fundamentals of Nursing
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• v.13 no.2
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• pp.217-224
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• 2006

Purpose: This study was done to investigate the effects of pilocarpine mouth care on the condition and discomfort of the oral cavity in patients with terminal cancer. Method: A quasi-experimental design with a non-equivalent control group, pre- and post-test was used. The participants were 30 patients admitted to the hospice care unit of C university hospital. Fourteen patients received pilocarpine mouth care for 5 days. The other sixteen received general mouth care. Results: Improvement in the condition of the oral cavity was significantly higher in the experimental group compared to the control group. Decrease in oral discomfort scores was significantly higher in the experimental group compared to the control group. The incidence of oral candidiasis was significantly higher in the control group compared to the experimental group. Conclusion: These findings indicate that pilocarpine mouth care could be an effective intervention for relieving oral discomfort, improving the condition of the oral cavity, and decreasing the incidence of oral candidiasis in patients with terminal cancer.

• Bulletin of the Korean Chemical Society
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• v.15 no.8
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• pp.680-684
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• 1994

Pilocarpine analogs were prepared by empoying a radical cyclization reaction as a key step for the five-membered ring formation.

• Journal of Oral Medicine and Pain
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• v.42 no.3
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• pp.72-80
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• 2017

Purpose: Pilocarpine as a salivation stimulant in pill form has mostly been used to relieve oral dryness for xerostomic patients but its use may often be limited due to variable side effects from systemic absorption. Therefore, the purpose of this study was to investigate the effects of pilocarpine mouthwash on salivation according to the variable concentration and duration for healthy volunteers. Related adverse effects and subjective assessment on its effects on salivation were also examined. Methods: This study was performed as placebo-controlled, double-blind, randomized clinical trial. Thirty healthy volunteers (male=23, mean age=22.2 years) were randomly allocated to 6 groups with the different concentration of pilocarpine mouthwash (placebo, 0.1%, 0.5%, 1.0%, 1.5%, and 2.0%). The whole experiment consisted of 3 sessions according to the duration of mouthwash, i.e., 1, 3, and 5 minutes with the mean wash-out period ${\geq}2$ days between the sessions. Unstimulated whole saliva was collected before and after gargling with a mouthwash. Results: Salivation of the higher concentration groups ${\geq}1%$ significantly increased than those of lower concentration group. The application period of mouthwash did not cause any changes of salivary flow rate at the higher concentrations ${\geq}1.0%$. The lower concentrations of 0.5% and 0.1% had no effects on salivation even after 5-minute mouthwash. There was no significant difference between blood pressure and pulse rate before and after use of mouthwash. Conclusions: From the results of the current study, pilocarpine mouthwash with at least 1.0% concentration more than a minute might be clinically effective in salivation without any serious side effects. Dose of mouthwash rather than duration seems to be a critical factor to salivation.

• Microbiology and Biotechnology Letters
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• v.41 no.2
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• pp.236-241
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• 2013

Pilocarpine is an imidazole alkaloid, found exclusively in the Pilocarpus genus, with huge pharmaceutical importance. In order to extract pilocarpine from Pilocarpus jaborandi, environmentally friendly enzyme-assisted extraction was applied. Viscozyme$^{(R)}$ L, a commercially available enzyme cocktail, was used for the study. The conditions for extraction were optimized on the basis of substrates, enzymes, temperatures and pHs. Optimum conditions for extraction with the highest yield were 30 h reaction of 100 mg substance at $45^{\circ}C$ in 40 ml of 50 mM acetic acid, pH 4. A 10% enzyme concentration was found to be the best for extraction. Total pilocarpine content after extraction was analyzed by HPLC. The total pilocarpine content ($1.14{\mu}g/mg$) obtained from Viscozyme$^{(R)}$ L treatment was 3.08-fold greater than those of the control treatment ($0.37{\mu}g/mg$).

• BMB Reports
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• v.53 no.4
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• pp.234-239
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• 2020

Epilepsy is a chronic neurological disease characterized by spontaneous recurrent seizures and caused by various factors and mechanisms. Malfunction of the olfactory bulb is frequently observed in patients with epilepsy. However, the morphological changes in the olfactory bulb during epilepsy-induced neuropathology have not been elucidated. Therefore, in the present study, we investigated the expression of parvalbumin (PV), one of the calcium-binding proteins, and morphological changes in the rat main olfactory bulb (MOB) following pilo-carpine-induced status epilepticus (SE). Pilocarpine-induced SE resulted in neuronal degeneration in the external plexiform layer (EPL) and glomerular layer (GL) of the MOB. PV immunoreactivity was observed in the neuronal somas and processes in the EPL and GL of the control group. However, six hours after pilocarpine administration, PV expression was remarkably decreased in the neuronal processes compared to the somas and the average number of PV-positive interneurons was significantly decreased. Three months after pilocarpine treatment, the number of PV-positive interneurons was also significantly decreased compared to the 6 hour group in both layers. In addition, the number of NeuN-positive neurons was also significantly decreased in the EPL and GL following pilocarpine treatment. In double immunofluorescence staining for PV and MAP2, the immunoreactivity for MAP2 around the PV-positive neurons was significantly decreased three months after pilocarpine treatment. Therefore, the present findings suggest that decreases in PV-positive GABAergic interneurons and dendritic density in the MOB induced impaired calcium buffering and reciprocal synaptic transmission. Thus, these alterations may be considered key factors aggravating olfactory function in patients with epilepsy.

• Annals of Clinical Neurophysiology
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• v.5 no.2
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• pp.171-176
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• 2003

Backgrounds and Objectives: Despite of enormous clinical and laboratory researches focused on the useful markers in status epilepticus(SE), clinically applicable methods are not yet available. Although ketogenic diet (KD) is an old method of treating epilepsies, its outstanding antiepileptic effect in some epileptic patients needs re-evaluation of this methods. This study was performed to evaluate the effect of KD on the change of nitric oxide(NO) during the SE. Methods: After the determination of critical EEG stages in the pilocarpine-induced SE model, serum NO levels were measured with Griess reaction. Open cardiac puncture was done immediately after the four different EEG stages of SE in the KD rats and regular diet (RD) rats. Cessation of SE was done with the 10~20 mg/Kg of diazepam i.p. injection in each stages of SE in KD and RD rats. Results: Pilocarpine-induced SE showed reliable EEG and behavioral patterns in all rats. Also, KD did not affect the SE induced by pilocarpine in terms of the SE induction time and SE severity. Serum NO was consistently higher in KD rats than RD rats in all SE stages. Conclusions: KD significantly increases NO during the pilocarpine-induced SE. These finding might contribute the neuroprotective effect of KD in the SE.

• The Korean Journal of Physiology
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• v.8 no.2
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• pp.49-53
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• 1974

A single dose of pilocarpine was subcutaneously injected into the rabbit in order to clarify the effects of cholinergic activities on the secretion of the pulmonary surfactant. The animal was sacrificed four hours after the injection, and the pressure-volume curve of the excised lung was obtained. The surfactant activities of the lung washings were also measured, and a comparison was made with the normal. The pressure-volume curve of the excised lung by the injection and ejection of air formed a loop (hysteresis) and the mean intra-alveolar pressure at 35 ml of air was 220 $mmH_20$ in the normal. The mean deflation curve of the pilocarpine treated rabbit lungs was shifted to the left compared with the normal. The surfactant activities were slightly increased than the normal. The above results suggest that pilocarpine stimulates the secretion of the pulmonary surfactant from the Type II alveolar epithelial cell.

• Journal of Life Science
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• v.30 no.6
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• pp.513-521
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• 2020

B-cell-specific Moloney murine leukemia virus integration site 1 (Bmi1) is a polycomb group protein and a core component of polycomb repressive complex 1. Initial research into Bmi1 has focused on its role in tumorigenesis, and it is generally accepted that it is important for the proliferation and survival of cancer cells. However, more recent studies have revealed that Bmi1 is downregulated in brains with neurodegenerative disease and that it regulates the function of mitochondria and reactive oxygen species levels. In this study, we tested the therapeutic potential of Bmi1 in pilocarpine-induced seizures in Bmi1-knockout mice. Bmi1 expression transiently increased in the hippocampal CA1 and CA3 and the dentate gyrus following pilocarpine-induced status epilepticus (SE). In terms of seizure behavior, SE induction was 43.14% and 53.57% for Bmi1^+/+ and Bmi1^+/- mice, respectively. However, there was no significant difference in mortality or hippocampal damage between the two groups. Two months after SE induction, the frequency of epileptic seizures in the Bmi1^+/- mice was 50% lower than in the control group, although the difference was not statistically significant. In addition, mossy fiber outgrowth in the Bmi1^+/- mice was significantly higher than in their wild-type littermates. Taken together, these data indicate that reduced Bmi1 activity increases pilocarpine-induced seizure probability and mossy fiber outgrowth.