• The Korean Journal of Physiology
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• v.14 no.1
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• pp.1-5
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• 1980

This study was under taken to investigate the influences of predictable or unpredictable stress upon gastric ulceration, and the hippocampectomy upon the ulceration order the stressful conditions. Sixty male albino rats(Sprague-Dawley strain) were divided equally into 3 groups: One was the hippocampal group(N=20) which received hippocampal ablation by suction, another was the cortical control group(N =20) which received partial cortical ablation over the hippocampus, and a third was the normal control group(N=20). Each group was further divided into two subgroups: One was the predicted subgroup(N=10) in which animals could predict the imminent stressful stimuli by hearing a sound(1,000 Hz, 2 sec in duration) 3 sec before the onset of the stress, and the other was the unpredicted subgroup(N=10). After starvation for 24 hours, but water ad libitum, each rat received the electric stimulation(3 mA, 60 Hz, 2 sec in duration, and once per minute in average) for 6 hours via a pair of electrodes attached on the tale. The electric stimulation served as the stress causing the gastric ulcer. Five hours after completion of stimulation, the stomach filled with the physiological saline was removed under deep anesthesia and spread out on a small glass plate. The numbers of the ulcer in each stomach were counted and the shape was examined under the dissecting microscope. Results obtained were as follows: 1. The mean numbers of the ulcer of the predicted subgroups were significantly larger than those of the unpredicted subgroups in the normal control and the cortical control groups, but there was no difference between the values of the two subgroups in the hippocampal group. 2. The mean numbers of the ulcer of the predicted subgroups in the normal control and the cortical control groups were larger(but not significant) than that in the hippocampal group. It is inferred from the above results that the prediction of the stress strengthens the effect of the stress on the gastric ulceration, and the hippocampus facilitates the effect of the prediction of the stress.

• Clinical and Experimental Reproductive Medicine
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• v.40 no.4
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• pp.155-162
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• 2013

Objective: Stress is known to be an inhibitor of the reproductive hypothalamic-pituitary-gonadal (HPG) axis. However, the neural and molecular connections between stress and reproduction are not yet understood. It is well established that in both humans and rodents, kisspeptin (encoded by the kiss1 gene) is a strong stimulator of the HPG axis. In the present study we hypothesized that endocannabinoids, an important neuromodulatory system in the brain, can act on the HPG axis at the level of kiss1 expression to inhibit reproductive function under stress. Methods: Adult male Wistar rats were unilaterally implanted with an intracerebroventricular cannula. Afterwards, the animals were exposed to immobilization stress, with or without the presence of the cannabinoid CB1 receptor antagonist AM251 (1 ${\mu}g/rat$). Blood samples were collected through a retro-orbital plexus puncture before and after stress. Five hours after the stress, brain tissue was collected for reverse transcriptase-quantitative polymerase chain reaction measurements of kiss1 mRNA. Results: Immobilization stress (1 hour) resulted in a decrease in the serum luteinizing hormone concentration. Additionally, kiss1 gene expression was decreased in key hypothalamic nuclei that regulate gonadotrophin secretion, the medial preoptic area (mPOA), and to some extent the arcuate nucleus (ARC). A single central administration of AM251 was effective in blocking these inhibitory responses. Conclusion: These findings suggest that endocannabinoids mediate, at least in part, immobilization stress-induced inhibition of the reproductive system. Our data suggest that the connection between immobilization stress and the HPG axis is kiss1 expression in the mPOA rather than the ARC.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1604-1611
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• 2006

Ostreae concha is natural products of sea that haves good function for anti-stress. WE observed the effect of Otreae concha, Yukkwooltang and yukwool-tang add Ostreae concha for catecholamine, GOT, GPT, LDH and TG after immobilization stress, Ostreae concha depressed the stress response. In immunohistochemical analysis, The area of withe pulp of the spleen decreased in the control groups as compared with control ones. At same time, more severe histological changes of spleen such as the decreased diameter of periarterial lymphoid sheath and splenic node were demonstrated in the rats challenged with emotional stress. But these changes were slightly recovered in rats pretreated with Sample I, Sample II and Sample III. Immunohistochemical analysis showed that the expression of the inflammation-related protein tended to increase. But a decline of these expression, especially TNF-${\alpha}$ by pretreated with Sample I, were observed in the red pulp of spleen of the experimental rats. These results suggest that ostreae concha may act as a therapeutic agent for stress disease through a regulation of stress-related hormones.

• Tuberculosis and Respiratory Diseases
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• v.68 no.2
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• pp.55-61
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• 2010

Background: The underlying pathogenesis of fat embolism-induced acute lung injury (ALI) has not been elucidated. In the present study, the pathogenesis of fat embolism-induced ALI was probed in association with neutrophilic oxidative stress in oleic acid (OA)-induced ALI of S-D rats. Methods: OA was injected intravenously to provoke ALI in experimental rats. Five hours later, indices of ALI were measured to confirm the role of the neutrophilic respiratory burst. The effect of an inhibition of phospholipase A2 (PLA2) was also evaluated. Results: The accumulation of neutrophils in the lung due to OA caused increased neutrophilic oxidative stress in lung, which was ameliorated by mepacrine. What were the results from inhibition of PLA2. Conclusion: Excess neutrophilic oxidative stress contributes to OA-induced ALI, which is lessened by the inhibition of PLA2.

• Molecules and Cells
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• v.46 no.12
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• pp.727-735
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• 2023

Stem cells require high amounts of energy to replicate their genome and organelles and differentiate into numerous cell types. Therefore, metabolic stress has a major impact on stem cell fate determination, including self-renewal, quiescence, and differentiation. Lysosomes are catabolic organelles that influence stem cell function and fate by regulating the degradation of intracellular components and maintaining cellular homeostasis in response to metabolic stress. Lysosomal functions altered by metabolic stress are tightly regulated by the transcription factor EB (TFEB) and TFE3, critical regulators of lysosomal gene expression. Therefore, understanding the regulatory mechanism of TFEB-mediated lysosomal function may provide some insight into stem cell fate determination under metabolic stress. In this review, we summarize the molecular mechanism of TFEB/TFE3 in modulating stem cell lysosomal function and then elucidate the role of TFEB/TFE3-mediated transcriptional activity in the determination of stem cell fate under metabolic stress.

• Biomedical Science Letters
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• v.25 no.3
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• pp.211-217
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• 2019

Research has established a strong connection between a diet rich in antioxidants and a decreased incidence of cardiovascular disease and cancer. These diets prominently feature fruits and vegetables containing high amounts of vitamins A, B, C and E, carotenoids, and minerals. Different processing conditions for these foods can alter their nutrient complement and potency. This study compared the antioxidant properties of a range of processed fruits and vegetables to see which yielded the highest level of antioxidant activity. We used an acetaminophen-induced oxidative stress mouse model to evaluate the antioxidant effects of extracts of processed apple, pear, carrot, cabbage, broccoli, and radish. Our results showed that the administration of these fruits decreased the expression of oxidative stress indicators such as ALT, AST, catalase, superoxide dismutase, GPx, and 8-OHdG. They also significantly protected mice livers from APAP-induced damage, as shown by histological evaluation. Our results have demonstrated the positive effects of processed fruits and vegetables in a mouse model of oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.555-563
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• 1999

It is well known that stress induces analgesia. This study was designed to demonstrate the stress-induced analgesia by employing hemorrhage and restraint and to investigate its mechanism and sex difference. The degree of pain was assessed by measuring the magnitude of jaw opening reflex produced by a noxious electrical stimulation in the dental pulp and by measuring the latency to withdraw the tail from a heat ray. Restraint showed an antinociceptive response. A significant increase in pain threshold on bleeding was shown and the increase was larger in male group than in female group. The tail flick latency (TFL) on bleeding after AVP antagonist injection into the ventricle was decreased and the decrease was greater in male rats than in female rats. Castration resulted in a significant reduction of TFL. This effect was reversed by treatment with sex hormones. TFL was decreased during hemorrhage in castrated rats. This response was opposite to that in non-castrated rats. TFL was further decreased during hemorrhage after infusion of AVP antagonist, and there was a significant sex difference. These results suggest that both restraint and hemorrhage produce an antinociception and that, in hemorrhage-induced analgesia, AVP and sex hormones may play an important role and male rats show a greater analgesic response.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.297.3-298
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• 2002

A benzopyranyl derivative. KR32000. synthesized as a plausible KATP opener. has been shown to exert cardioprotective effect in vivo myocardial infarct model. In this study. we investigated whether KR32000 can produce cardioprotective effect against hypoxia- and reactive oxygen species(ROS)-induced injury in heart-derived H9c2 cells. Hypoxic injury was induced by incubating cells in anaerobic chamber (glucose-free. serum-free DMEM. 85% N2. 5% CO2. 10% H2) and oxidative stress was induced by buthionine sulfoximine(BSO). (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.3
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• pp.263-273
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• 1999

The role of phospholipase $A_2\;(PLA_2)$ in acute lung leak induced by intestinal ischemia was investigated in association with neutrophilic respiratory burst. To induce lung leak, we generated intestinal ischemia for 60 min prior to the 120 min reperfusion by clamping superior mesenteric artery in Sprague-Dawley rats. Acute lung leak was confirmed by the increased lung leak index and protein content in bronchoalveolar fluid. These changes were inhibited by mepacrine, the non-specific $PLA_2$ inhibitor. The lung myeloperoxidase (MPO) activity denoting the pulmonary recruitment of neutrophils was increased by intestinal I/R, but decreased by mepacrine. Simultaneously, the number of leukocytes in bronchoalveolar fluid was increased by intestinal ischemia/reperfusion (I/R) and decreased by mepacrine. Gamma glutamyl transferase activity, an index of oxidative stress in the lung, was increased after intestinal I/R but decreased by mepacrine, which implicates that $PLA_2$ increases oxidative stress caused by intestinal I/R. The $PLA_2$ activity was increased after intestinal I/R not only in the intestine but also in the lung. These changes were diminished by mepacrine. In the cytochemical electron microscopy to detect hydrogen peroxide, intestinal I/R increased the generation of the hydrogen peroxide in the lung as well as in the intestine. Expression of interleukin-1 (IL-1) in the lung was investigated through RT-PCR. The expression of IL-1 after intestinal I/R was enhanced, and again, the inhibition of $PLA_2$ suppressed the expression of IL-1 in the lung. Taken together, intestinal I/R seems to induce acute lung leak through the activation of $PLA_2$, the increase of IL-1 expression associated with increased oxidative stress by neutrophilic respiratory burst.

• Molecules and Cells
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• v.27 no.3
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• pp.279-282
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• 2009

"Two-cysteine" peroxiredoxins are antioxidant enzymes that exert a cytoprotective effect in many models of oxidative stress. However, under highly oxidizing conditions they can be inactivated through hyperoxidation of their peroxidatic active site cysteine residue. Sulfiredoxin can reverse this hyperoxidation, thus reactivating peroxiredoxins. Here we review recent investigations that have shed further light on sulfiredoxin's role and regulation. Studies have revealed sulfiredoxin to be a dynamically regulated gene whose transcription is induced by a variety of signals and stimuli. Sulfiredoxin expression is regulated by the transcription factor AP-1, which mediates its up-regulation by synaptic activity in neurons, resulting in protection against oxidative stress. Furthermore, sulfiredoxin has been identified as a new member of the family of genes regulated by Nuclear factor erythroid 2-related factor (Nrf2) via a conserved cis-acting antioxidant response element (ARE). As such, sulfiredoxin is likely to contribute to the net antioxidative effect of small molecule activators of Nrf2. As discussed here, the proximal AP-1 site of the sulfiredoxin promoter is embedded within the ARE, as is common with Nrf2 target genes. Other recent studies have shown that sulfiredoxin induction via Nrf2 may form an important part of the protective response to oxidative stress in the lung, preventing peroxiredoxin hyperoxidation and, in certain cases, subsequent degradation. We illustrate here that sulfiredoxin can be rapidly induced in vivo by administration of CDDO-TFEA, a synthetic triterpenoid inducer of endogenous Nrf2, which may offer a way of reversing peroxiredoxin hyperoxidation in vivo following chronic or acute oxidative stress.