• 대한약리학회지
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• 제29권2호
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• pp.195-202
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• 1993

스트렙토조토신으로 당뇨를 유발시킨 쥐의 심근 근장그물에서 칼슘이동이 저하됨을 볼 수 있었다. 칼슘이동의 저하는 최대칼슘 uptake의 감소와 칼슘에 대한 affinity의 감소로 나타났다. 이러한 심근 근장그물의 기능저하가 나타나는 작용기전이 심근 근장그물 단백의 산화성 손상과 관계가 있는지를 살펴보았다. 당뇨쥐에서는 glycohemoglobin과 carbonyl group의 양이 현저히 증가됨을 볼 수 있었다. 한편으로 cyclic AMP 의존성 protein kinase의 catalytic subunit에 의한 phospholamban 인산화에 의해 심근 근장고물 칼슘이동의 증가를 보였고, 이 증가는 대조군에 비하여 당뇨군에서 훨씬 현저하게 나타났다. SDS-polyacrylamide를 이용한 전기영동후 autoradiogram을 통하여 확인한 phospholamban 인산화는 당뇨군에서 진한 band로 나타남이 확인되었다. 이상의 결과로 미루어 당뇨군의 심근 근장그물 기능저하는, 기초상태에서 아마도 심근내 저하된 norephinephrine 양으로 인하여 phospholamban 인산화 정도가 적으므로 근장그물 $Ca^{2+}-ATPase$ 억제가 나타남을 제시해 주며, 근장그물 단백의 산화성 손상도 당뇨성 심근질한을 일으킬 수 있는 또 다른 요인 중의 하나로 생각된다.

• 한국양식학회지
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• 제6권2호
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• pp.107-123
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• 1993

조피볼락의 필수지방산인 n-3HUFA가 어체에 미치는 생화학적 변화를 알아보기 위하여, n-3HUFA 함량이 $0.0\~1.5\%$가 되도록 조정한 6종의 실험사료로 조피볼락 치어를 10주간 사육하여 혈액성상, 혈청성분 및 간세포 성상의 변화를 검토하였다. 혈액성상(RBC, Hb, Ht, MCV, MCHC 및 MCH)은 사료의 n-3HUFA 함량에 따라 유의적인 차이를 나타내지는 않았다. 혈청단백질 농도$(2.76\~3.63g/100ml)$ 및 혈당량$(36\~71mg/100ml)$은 n-3HUFA $0.9\%$ 사료까지는 증가하다가 그 이상에서는 일정한 값을 유지하였다. 혈중 total cholesterol 농도$(137\~86mg/100ml)$와 free cholesterol 농도$(84.2\~63.8mg/100ml)$는 n-3HUFA $1.2\%$까지 점차 감소하는 경향을 보였으며, 그 이상에서는 일정 하였다. 혈청 GPT $(159.7\~47.0 Karmen\; unit)$, GOT $(28.0\~11.1\;Karmen\;unit)$ 및 LDH $(3888\~1539\;W-unit)$도 모두 n-3HUFA $1.2\%$까지는 감소 경향을 보이다가 그 이후에는 일정한 값을 유지하였다. n-3HUFA 무첨가 사료를 먹은 실험어의 간조직은 n-3HUFA $1.5\%$ 첨가 사료를 먹은 실험어에 비해 인포색의 구조 붕괴와 부분적인 세포 융해가 관찰되었다. 간 cytosol의 LDH 활성과 microsomal membrane의 $Ca^{2+}-ATPase$ 활성도 변화되어 사료의 n-3HUFA가 증가할수록 증가한 경향을 보였다.

• 한국식품과학회지
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• 제16권3호
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• pp.353-357
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• 1984

PSE돈육에서 근원섬유를 추출하고, 무수석시닐산으로 수식하여 석시닐화하고, 그 조제물의 화학적, 기능적 특성을 검토하였다. 석시닐화근원섬유는 석시닐화율에 상관없이 효소적 기능이 완전히 상실하였고, 무처리근원섬유의 등전점이 pH 5.0인데 비하여 석시닐화근원섬유는 pH 3.0정도에서 침전하였다. 염농도에 따른 용해도는 무처리근원섬유가 염농도의존성이 있음에 비하여 석시닐화근원섬유는 염농도에 관계없이 용해도의 변화가 거의 없었다. 석시닐화근원섬유의 기능적 특성중 열응고성은 현저히 감소하였고, 흡수성은 개선되지 않았으며, 유화용량은 다소 향상되었다.

• 대한의생명과학회지
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• 제27권3호
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• pp.170-176
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• 2021

Thapsigargin (TG), a sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase (SERCA) inhibitor, has been widely used as an agonist for platelet aggregation for decades. In this study, we investigated the effect of TG on the release of lactate dehydrogenase (LDH) for platelets and elucidated its mechanism. Platelet LDH release and platelet aggregation were increased by TG treatment; 1,000 nM of TG induced the complete lysis of platelets. Other agonists such as collagen (2.5 ㎍/mL), thrombin (0.1 U/mL), and ADP (10 mM) did not induce significant platelet LDH release despite platelet aggregation. Finally, we investigated the effects of pharmacological inhibitors on TG-induced platelet aggregation and LDH release. SP600125, a JNK inhibitor, and LY294002, a PI-3K inhibitor, inhibited TG-induced platelet LDH release but not platelet aggregation. Forskolin, an adenylyl cyclase activator, also inhibited LDH release without affecting platelet aggregation by TG. These results suggest that the TG-induced platelet aggregation was accompanied by LDH release but regulated by a different signaling pathway.

• Journal of Animal Science and Technology
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• 제65권2호
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• pp.336-350
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• 2023

Two experiments were conducted in this research. Experiment 1 investigated the spatial expression characteristics of calcium (Ca) and phosphorus (P) transporters in the duodenum, jejunum, and ileum of 21-day-old broilers provided with adequate nutrient feed. Experiment 2 evaluated the effects of dietary vitamin D₃ (VD₃) concentration (0, 125, 250, 500, 1,000, and 2,000 IU/kg) on growth performance, bone development, and gene expression levels of intestinal Ca and P transporters in 1-21-day-old broilers provided with the negative control diet without supplemental VD₃. Results in experiment 1 showed that the mRNA levels of calcium-binding protein 28-kDa (CaBP-D28k), sodium-calcium exchanger 1 (NCX1), plasma membrane calcium ATPase 1b (PMCA1b), and IIb sodium-phosphate cotransporter (NaPi-IIb) were the highest in the broiler duodenum. By contrast, the mRNA levels of inorganic phosphate transporter 1 (PiT-1) and 2 (PiT-2) were the highest in the ileum. Results in experiment 2 showed that adding 125 IU/kg VD₃ increased body weight gain (BWG), feed intake (FI), bone weight, and percentage and weight of Ca and P in the tibia and femur of 1-21-day-old broilers compared with the negative control diet (p < 0.05). The rise in dietary VD₃ levels from 125 to 1,000 IU/kg further increased the BWG, FI, and weights of the bone, ash, Ca, and P (p < 0.05). No difference in growth rate and leg bone quality was noted in the broilers provided with 1,000 and 2,000 IU/kg VD₃ (p > 0.05). Supplementation with 125-2,000 IU/kg VD₃ increased the mRNA abundances of intestinal Ca and P transporters to varying degrees. The mRNA level of CaBP-D28k increased by 536, 1,161, and 28 folds in the duodenum, jejunum, and ileum, respectively, after adding 1,000 IU/kg VD₃. The mRNA levels of other Ca and P transporters (PMCA1b, NCX1, NaPi-IIb, PiT-1, and PiT-2) increased by 0.57-1.74 folds by adding 1,000-2,000 IU/kg VD₃. These data suggest that intestinal Ca and P transporters are mainly expressed in the duodenum of broilers. Moreover, the addition of VD₃ stimulates the two mineral transporter transcription in broiler intestines.

• 대한약침학회지
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• 제16권1호
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• pp.43-49
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• 2013

Objective: Pyungwi-san (PWS) plays a role in a number of physiologic and pharmacologic functions in many organs. Interstitial cells of Cajal (ICCs) are pacemaker cells that generate slow waves in the gastrointestinal (GI) tract. We aimed to investigate the beneficial effects of PWS in mouse small-intestinal ICCs. Methods: Enzymatic digestion was used to dissociate ICCs from the small intestine of a mouse. The whole-cell patch-clamp configuration was used to record membrane potentials from the cultured ICCs. Results: ICCs generated pacemaker potentials in the GI tract. PWS produced membrane depolarization in the current clamp mode. Pretreatment with a $Ca^{2+}$-free solution and a thapsigargin, a $Ca^{2+}$-ATPase, inhibitor in the endoplasmic reticulum, eliminated the generation of pacemaker potentials. However, only when the thapsigargin was applied in a bath solution, the membrane depolarization was not produced by PWS. Furthermore, the membrane depolarizations due to PWS were inhibited not by U-73122, an active phospholipase C inhibitor, but by chelerythrine and calphostin C, protein kinase C inhibitors. Conclusions: These results suggest that PWS might affect GI motility by modulating the pacemaker activity in the ICCs.

• 대한약리학회지
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• 제8권2호
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• pp.55-61
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• 1972

Superprecipitation of actomyosin has been considered to be an in vitro model of the muscle contraction. The superprecipitation and ATPase activity (which supplies the energy for contraction) are influenced by several factors which are the large amount of changes in ionic strength, Mg and ATP concentrations. But those behaviors are found to be promptly influenced by the change in a small range of calcium concentration which can be controlled by the cellular function of muscle physiologically only in the presence of the modullatory proteins, tropomyosin and troponin. In order to elucidate the precise roles of calcium in the muscle contraction and relaxation, the effects of calcium on the actin- myosin interaction was observed in the presence of tropomyosin and troponin using the superprecipitation system. The results are summarized as follows: 1. EGTA (glycol ether diaminetetraacetic acid)prolonged the initiation of the superprecipitation of natural actomyosin. 2. Superprecipitation curve was declined by adding EGTA at the time when tile curve reached the half- maximum. The degree of declining was proportional to the amount of EGTA added. Especially, upon adding 0.25 mM EGTA the curve was lowered to the level before the protein superprecipitated. But addition of EGTA did not affect the curve after attaining the maximum. 3. Superprecipitation of Perry myosin B was not affected by EGTA added both before and during the course of the reaction. 4. Tropomyosin did not change the response of Perry myosin B to EGTA added at any time of the reaction. 5. Troponin also did not change the response of Perry myosin B to EGTA. 6. Both tropomyosin and troponin together rendered the Perry myosin B to obtain the same response as natural actomyosin to EGTA. 7. It was concluded that actin-myosin interaction was influenced by the minute change of calcium concentration only in the presence of both tropomyosin and troponin. We could reproduce the contraction and relaxation of the muscle in vitro under the presence of ATP by changing the calcium concentration.

• Clinical and Experimental Reproductive Medicine
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• 제32권4호
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• pp.337-346
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• 2005

Objective: The oligosaccharide moieties of glycoproteins and proteoglycans have a vital function in blastocyst differentiation. Concanavalin (ConA), a lectin, is known to bind on the preimplantation embryos, especially on blastocyst. In this study, we investigated whether ConA can modulate the trophoblast development and about the regulating mediator. Also, we investigated whether expansion is enough for hatching procession of the mouse blastocyst. Method: Embryos were collected at 72 h post hCG injection and chemicals were treated after 24 h (96 hr post hCG injection). ConA or calcium ionophore A23187 were exposed to blastocyst and than analysis the developmental process for 48 hr. Intracellular free-$Ca^{2+}$ concentration in trophectoderm was measured with confocal laser microscope after exposing to ConA or calcium ionophore A23187. ConA-pretreated blastocyst exposed to the calcium ionophore A23187 and then analyzed the developmental process. Otherwise ouabain was treated to the blastocyst to block the $Na^+/K^+$-ATPase activity. Results: In contrast to the control blastocyst, the ConA-exposed blastocysts developed beyond the expansion stage with significantly high rate (90.4%) at 12 h post administration. ConA induced an increase the intracellular $Ca^{2+}$ concentration in trophectoderm. Calcium ionophore A23187 also stimulated expansion of blastocyst. Most of the control blastocysts developed to the hatching stage at 144 h post hCG injection. However, strongly 65% of the ConA-exposed embryos were arrested at expanded stage at same time point. The developmental progression rates to hatching stage of both ConA- and calcium ionophore A23187-expose blastocysts were significantly lower than that of the control. However ConA-pretreated embryos developed to the hatching stage like control embryos. Ouabain showed a tendency to delayed the progress to expansion stage but did not inhibit the development to the hatching stage. Conclusion: ConA-mediated expansion is the result of the increase of intracellular free-calcium in blastocyst stage embryo. It is suspected that expansion of the blasocyst is a essential indirect factor in hatching and the calcium may triggering the cellular mechanisms for the both expansion and hatching progression.

• Archives of Pharmacal Research
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• 제29권5호
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• pp.375-383
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• 2006

The anti platelet effects of a novel guanidine derivative, KR-32570 ([5-(2-methoxy-5-chlorophenyl) furan-2-ylcarbonyl]guanidine), were investigated with an emphasis on the mechanisms underlying its inhibition of collagen-induced platelet aggregation. KR-32570 significantly inhibited the aggregation of washed rabbit platelets induced by collagen $(10{\mu}g/mL)$, thrombin (0.05 U/mL), arachidonic acid $(100{\mu}M)$, a thromboxane (TX) $A_2$ mimetic agent U46619 (9,11-dideoxy-9,11-methanoepoxy-prostaglandin $F_2,\;1{\mu}M$) and a $Ca^{2+}$ ATPase inhibitor thapsigargin $(0.5{\mu}M)$ ($IC_{50}$ values: $13.8{\pm}1.8,\;26.3{\pm}1.2,\;8.5{\pm}0.9,\;4.3{\pm}1.7\;and\;49.8{\pm}1.4{\mu}M$, respectively). KR-32570 inhibited the collagen-induced liberation of $[^3H]$arachidonic acid from the platelets in a concentration dependent manner with complete inhibition being observed at $50{\mu}M$. The $TXA_2$ synthase assay showed that KR-32570 also inhibited the conversion of the substrate $PGH_2$ to $TXB_2$ at all concentrations. Furthermore, KR-32570 significantly inhibited the $[Ca^{2+}]_i$ mobilization induced by collagen at $50{\mu}M$, which is the concentration that completely inhibits platelet aggregation. KR-32570 also decreased the level of collagen $(10{\mu}g/mL)$induced secretion of serotonin from the dense-granule contents of platelets, and inhibited the NHE-1-mediated rabbit platelet swelling induced by intracellular acidification. These results suggest that the antiplatelet activity of KR-32570 against collagen-induced platelet aggregation is mediated mainly by inhibiting the release of arachidonic acid, $TXA_2$ synthase, the mobilization of cytosolic $Ca^{2+}$ and NHE-1.

• The Korean Journal of Physiology and Pharmacology
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• 제11권4호
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• pp.149-154
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• 2007

Kainic acid (KA) causes neurodegeneration, but no consensus has been reached concerning its mechanism. Nitric oxide may be a regulator of the mechanism. We identified differentially expressed genes in the hippocampus of mice treated with kainic acid, together with or without L-NAME, a nonselective nitric oxide synthase inhibitor, using a new differential display PCR method based on annealing control primers. Eight genes were identified, including clathrin light polypeptide, TATA element modulatory factor 1, neurexin III, ND4, ATPase, $H^+$ transporting, V1 subunit E isoform 1, and N-myc downstream regulated gene 2. Although the functions of these genes and their products remain to be determined, their identification provides insight into the molecular mechanism(s) involved in KA-induced neuronal cell death in the hippocampal CA3 area.