• Fisheries and Aquatic Sciences
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• v.22 no.1
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• pp.2.1-2.9
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• 2019

In the present study, the protective effects of Hizikia fusiforme and Chlorella sp. extracts on lead acetate-induced hepatotoxicity were investigated. Hepatic damage was induced in rats by intraperitoneal (i.p.) injection of lead acetate and the protective effects of H. fusiforme (HZK) and Chlorella sp. (CHL) extracts on lead acetate-induced hepatic damage in rat liver were examined. The results revealed significantly increased glutamic oxaloacetate and glutamic pyruvic transaminase levels in the group treated with lead acetate only (Pb group); oral administration of HZK and CHL extracts tended to decrease the enzyme levels similar to those observed in the control group. Regarding antioxidant enzymes, superoxide dismutase activity was increased in the Pb group and decreased in a concentration-dependent manner in the HZK- and CHL-treated groups. Glutathione levels were increased in a concentration-dependent manner in the HZK- and CHL-treated groups. There was no significant difference in catalase activity. Western blot analysis showed inflammation-related protein expression in mitogen-activated protein kinase and Nrf2 pathways was affected in the HZK- and CHL-treated groups. Therefore, HZK and CHL extracts exerted antioxidant and anti-inflammatory effects against lead acetate-induced hepatotoxicity. Development of functional health foods containing HZK and CHL extracts, which have hepatoprotective effects against inhaled lead acetate, should be considered.

• The Korean Journal of Zoology
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• v.35 no.3
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• pp.277-286
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• 1992

개구리의 난자로 부터 maturation promoting factor(MPF)를 추출, 부분 분리하여 이들의 활성을 조사하고 이 물질의 생성과 protein kinase C(반KC)와의 관계를 조사하SB다. 성숙된 난자를 분쇄한 후 초원심분리과정을 거쳐 MPF의 crude extract(CE)를 얻은 다음 ultrafiltration (UF)과 고속액체크로마토그라피를 거쳐서 3종류의 분획 (peak 1, 11, and 111)을 얻었다. 이들 분획을 in nitro assay와 autoradiDgraphy를 사용하여 확인한 결과 분획 11에서 MPF 활성이 있는 것을 알았다. 분리 단계에 따라 MPF의 정제도를 Hl histone kinase assay로 조사한 결깍 UF를 거친 것은 CE보다 약 3배로, 분획 11에서는 약 117배로 증가한 것을 확인하였다. 또한 MPF분획의 인산화를 autoradiography로 조사한 결과 45 KD 단백질을 포함한 수종의 난자 단백질이 강하게 인산화되었음을 알 수 있었다. PKC의 활성화가 난자내 MPF의 생성을 유도하는가를 보기 위하여 PKC의 활성제인 12-0-tetradecanoyl phorbol 13 acetate(TPA)를 처리한 난자의 세포질 추출물을 미세주입 법으로 조사한 결과 TPA 처리 후 6시간부터 난자내 MPF의 활성이 나타나는 것을 알 수 있었다. 이러한 결과들은 PKC의 활성화가 MPF의 생성을 유도하고, MPF의 활성화와 함께 일부 단백질들의 인산화를 통하여 궁극적으로 난자 성숙을 촉진했음을 시사한다.

• Horticultural Science & Technology
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• v.31 no.6
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• pp.813-820
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• 2013

Monoterpenoids were recently found as main biologically active compounds which is responsible for various physiological effect in goat's beard (Aruncus dioicus). Ethyl acetate extract of A. dioicus (ADE) was treated to B16F10 melanoma cells for the examination of whitening activity. MTT assay was performed to evaluate cell toxicity and the result showed that slight cell toxicity (> 10%) by over $500{\mu}g{\cdot}mL^{-1}$. Thus, 0, 5, 10, or $50{\mu}g{\cdot}mL^{-1}$ ADE was used for further experiments. We found that tyrosinase activity was decreased according to ADE concentration, and the total melanin content was also dramatically reduced. Especially with $50{\mu}g{\cdot}mL^{-1}$ ADE treatment tyrosinase activity was reduced to 35.6%, and 58.8% of melanin content was lowered. In addition, whitening related proteins including tyrosinase, tyrosinase related protein 1 (TRP1), TRP2, microphthalmia associated transcription factor (MITF) and cAMP and protein kinase A (PKA) were reduced by ADE treatment. It caused decreased phosphorylation of cAMP response binding protein (CREB) but increased phosphorylation of extracellular signal related kinase (ERK). Therefore, in this paper we would like to suggest the potent usage of A. dioicus natively grown in Ulleungdo, Korea as materials of functional cosmetics by confirming whitening activity related with melanin content.

• Korean Journal of Pharmacognosy
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• v.44 no.4
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• pp.379-383
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• 2013

Portulaca oleracea L. is known to have many biological benefits such as anti-oxidant, anti-inflammatory, anti-allergic and anti-tumor. The objective of this study is to explore the neuroprotective effect of P. oleracea L. against glutamate-induced oxidative stress in mouse hippocampal HT22 cells. P. oleracea L. 70% ethanol extract and solvent fractions have the potent neroprotective effects on glutamate-induced nerotoxicity by induced the expression of heme oxygenase (HO)-1 in HT22 cells. Especially, ethyl acetate fraction showed higher protective effect. In HT22 cell, P. oleracea L. treatment with ERK inhibitor (PD98059) and c-JUN N-terminal kinase (JNK) inhibitor (SP600125) reduced P. oleracea L. ethyl acetate fraction induced HO-1 expression and P. oleracea L. ethyl acetate fraction also increased ERK and JNK phosphorylation. Furthermore, we found that treatment of P. oleracea L. caused the nuclear accumulation of Nrf2. In conclusion, the ethyl acetate fraction of 70% ethanol extract of P. oleracea L. significantly protect glutamate-induced oxidative damage by induction of HO-1 via Nrf2, ERK and JNK pathway in mouse hippocampal HT22. Taken together these finding suggest that P. oleracea L. ethyl acetate fraction is good source for taking active compounds and may be a potential therapeutic agent for brain disorder that induced by oxidative stress and neuronal damage.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.46 no.4
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• pp.384-392
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• 2013

An ethanolic extract of Undaria pinnatifida was fractionated using several solvents. Of the fractions, the ethyl acetate fraction had the greatest inhibitory effect on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 macrophage cells. Using this fraction (U. pinnatifida ethyl acetate extract, UPE), we investigated the molecular mechanism underlying its inhibitory effect on LPS-stimulated RAW 264.7 cells. Pretreatment of the cells with up to $100{\mu}g/mL$ UPE significantly inhibited NO production and inducible nitric oxide synthase (iNOS) expression, in a dose-dependent manner. Similarly, UPE treatment markedly reduced the production of pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6 and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), while it strongly suppressed the nuclear translocation of nuclear factor-kappa B (NF-${\kappa}B$) by preventing proteolytic degradation of inhibitor of nuclear factor ${\kappa}B$ $(I{\kappa}B)-{\alpha}$. Moreover, UPE treatment significantly reduced the phosphorylation of phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK) in LPS-stimulated cells. These results indicate that UPE contains anti-inflammatory compounds and suggest that it might be used as a functional food material that assists in prevention of inflammatory diseases.

• Animal Bioscience
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• v.35 no.9
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• pp.1444-1453
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• 2022

Objective: Acetate plays an important role in host lipid metabolism. However, the network of acetate-regulated lipid metabolism remains unclear. Previous studies show that mitogen-activated protein kinases (MAPKs) and mechanistic target of rapamycin (mTOR) play a crucial role in lipid metabolism. We hypothesize that acetate could affect MAPKs and/or mTOR signaling and then regulate lipid metabolism. The present study investigated whether any cross talk occurs among MAPKs, mTOR and acetate in regulating lipid metabolism. Methods: The ceramide C6 (an extracellular signaling-regulated kinases 1 and 2 [ERK1/2] activator) and MHY1485 (a mTOR activator) were used to treat rabbit adipose-derived stem cells (ADSCs) with or without acetate, respectively. Results: It indicated that acetate (9 mM) treatment for 48 h decreased the lipid deposition in rabbit ADSCs. Acetate treatment decreased significantly phosphorylated protein levels of ERK1/2 and mTOR but significantly increased mRNA level of hormone-sensitive lipase (HSL). Acetate treatment did not significantly alter the phosphorylated protein level of p38 MAPK and c-Jun aminoterminal kinase (JNK). Activation of ERK1/2 and mTOR by respective addition in media with ceramide C6 and MHY1485 significantly attenuated decreased lipid deposition and increased HSL expression caused by acetate. Conclusion: Our results suggest that ERK1/2 and mTOR signaling pathways are associated with acetate regulated HSL gene expression and lipid deposition.

• Molecules and Cells
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• v.24 no.1
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• pp.9-15
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• 2007

To investigate the effects of chitosan on the redifferentiation of dedifferentiated chondrocytes, we used chondrocytes obtained from a micromass culture system. Micromass cultures of chick wing bud mesenchymal cells yielded differentiated chondrocytes, but these dedifferentiated during serial monolayer subculture. When the dedifferentiated chondrocytes were cultured on chitosan membranes they regained the phenotype of differentiated chondrocytes. Expression of protein kinase $C{\alpha}$ ($PKC{\alpha}$) increased during chondrogenesis, decreased during dedifferentiation, and increased again during redifferentiation. Treatment of the cultures with phorbol 12-myristate 13-acetate (PMA) inhibited redifferentiation and down-regulated $PKC{\alpha}$. In addition, the expression of p38 mitogen-activated protein (MAP) kinase increased during redifferentiation, and its inhibition suppressed redifferentiation. These findings establish a culture system for producing chondrocytes, point to a new role of chitosan in the redifferentiation of dedifferentiated chondrocytes, and show that $PKC{\alpha}$ and p38 MAP kinase activities are required for chondrocyte redifferentiation in this model system.

• Archives of Pharmacal Research
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• v.18 no.4
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• pp.262-266
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• 1995

Bacterial lipopolysaccharide (LPS) is one of the most potent inducers of various cytokines nad other proinflammatory mediators in macrophages. Although pathophysiological consequences of LPS-induced responses are well established, the mechanisms through which LPS-generated singals are transduced remain unclear. In the present study, we attempted to determine early intracellular events after LPS binding which transduced the signal for the induction of arachidonic acid metabolism in rat alveolar macrophages. While H-7, a protein kinase C(PKC) inhibitor, did not affect LPS-stimulated prostaglandin synthesis, staurosporine enhanced archidonic acid etabolism in macropahages treated with LPS. Phorbol-12-myristate-13 acetate snesitive to LPS compare with control group. PMA and H-7 did not alter the effect of flucose. Pertussis toxin did not show nay effect, thus pertussis toxin snesitive G-protein pathway appears not to play a role in this experimental system. Genistein and tyrphostin 25, protein tyrosine kinase 9PTK) inhibitors, markedly inhibited prostaglandin synthesis in macrophages nal transduction events leading to icnreased macrophage arachidonic acid metabolism.

• Archives of Pharmacal Research
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• v.27 no.7
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• pp.757-762
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• 2004

The protective adaptive response to electrophiles and reactive oxygen species is mediated by the induction of phase II detoxifying genes including glutathione S-transferases (GSTs). NF-E2-related factor-2 (Nrf2) phosphorylation by protein kinase C (PKC) is a critical event for its nuclear translocation in response to oxidative stress. Previously, we have shown that peroxynitrite plays a role in activation of Nrf2 and Nrf2 binding to the antioxidant response element (ARE) via the pathway of phosphatidylinositol 3-kinase (PI3-kinase) and that nitric oxide synthase in hepatocytes is required for GSTA2 induction. In view of the importance of PKC and Pl3-kinase in Nrf2-mediated GST induction, we investigated the role of these kinases in peroxynitrite formation for GSTA2 induction by oxidative stress and determined the relationship between PKC and PI3-kinase. Although PKC activation by phorbol 12-myristate-13-acetate (PMA) did not increase the extents of constitutive and inducible GSTA2 expression, either PKC depletion by PMA or PKC inhibition by staurosporine significantly inhibited GSTA2 induction by tert-butylhydroquinone (t-SHa) a prooxidant chemical. Therefore, the basal PKC activity is req- uisite for GSTA2 induction. 3-Morpholinosydnonimine (SIN-1), which decomposes and yields peroxynitrite, induced GSTA2, which was not inhibited by PKC depletion, but slightly enhanced by PKC activation, suggesting that PKC promotes peroxynitrite formation for Nrf2-mediated GSTA2 induction. Treatment of cells with S-nitroso-N-acetyl-penicillamine (SNAP), an exogenous NO donor, in combination with t-BHQ may produce peroxynitrite. GSTA2 induction by SNAP ＋ t-BHQ was not decreased by PKC depletion, but rather enhanced by PKC activation, showing that the activity of PKC might be required for peroxynitrite formation. LY294002 a P13-kinase inhibitor blocked GSTA2 induction by t-BHQ, which was reversed by PMA-induced PKC activation. These results provide evidence that PKC may playa role in formation of peroxynitrite that activates Nrf2 for GSTA2 induction and that PKC may serve an activator for GSTA2 induction downstream of PI3-kinase.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.111-115
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• 2004

Roundabout (Robo) is the transmembrane receptor for slit, the neuronal guidance molecule. In this study, the tyrosine phosphorylation of Robo was observed in Robo-transfected human embryonic kidney cells and developing rat brains, and found to be increased by the treatment with protein kinase A activator, forskolin. In contrast, protein kinase C activation by phorbol-12-myristate-13-acetate decreased the phosphorylation of Robo. Intracellular calcium was required for the tyrosine phosphorylation. Furthermore, the transfection of an Eph receptor tyrosine kinase dramatically enhanced the tyrosine phosphorylation. These findings indicate that the tyrosine phosphorylation of Robo is regulated by multiple mechanisms, and that Eph receptor kinases may play a role in the regulation of tyrosine phosphorylation of Robo in the rat brain.