• IMMUNE NETWORK
• /
• 제24권2호
• /
• pp.17.1-17.16
• /
• 2024

We have reported that anterior cruciate ligament (ACL) injury leads to the differential dysregulation of the complement system in the synovium as compared to meniscus tear (MT) and proposed this as a mechanism for a greater post-injury prevalence of post traumatic osteoarthritis (PTOA). To explore additional roles of complement proteins and regulators, we determined the presence of decay-accelerating factor (DAF), C5b, and membrane attack complexes (MACs, C5b-9) in discarded surgical synovial tissue (DSST) collected during arthroscopic ACL reconstructive surgery, MT-related meniscectomy, osteoarthritis (OA)-related knee replacement surgery and normal controls. Multiplexed immunohistochemistry was used to detect and quantify complement proteins. To explore the involvement of body mass index (BMI), after these 2 injuries, we examined correlations among DAF, C5b, MAC and BMI. Using these approaches, we found that synovial cells after ACL injury expressed a significantly lower level of DAF as compared to MT (p<0.049). In contrast, C5b staining synovial cells were significantly higher after ACL injury (p<0.0009) and in OA DSST (p<0.039) compared to MT. Interestingly, there were significantly positive correlations between DAF & C5b (r=0.75, p<0.018) and DAF & C5b (r=0.64 p<0.022) after ACL injury and MT, respectively. The data support that DAF, which should normally dampen C5b deposition due to its regulatory activities on C3/C5 convertases, does not appear to exhibit that function in inflamed synovia following either ACL injury or MT. Ineffective DAF regulation may be an additional mechanism by which relatively uncontrolled complement activation damages tissue in these injury states.

• 대한약침학회지
• /
• 제21권3호
• /
• pp.159-167
• /
• 2018

Objectives: Myocardial reperfusion is the only logical cure for ischemic heart disease. However, ischemic-reperfusion (I/R) injury is one of the underlying factors facilitating and accelerating the apoptosis in the myocardium. This study set to investigate the impact of Teucrium polium (TP) hydro-alcoholic extract on I/R induced apoptosis in the isolated rat heart. Methods: Isolated rat hearts were classified into six groups. The control samples were subjected to 80 min of perfusion with Krebs-Henseleit bicarbonate (KHB) buffer; in control-ischemia group, after primary perfusion (20 min) the hearts were exposed to global ischemia (20 min) and reperfusion (40 min). Pretreated groups were perfused with $500{\mu}M$ of vitamin C and various TP concentrations (0.5, 1, 2 mg/ml) for 20 min, and then the hearts were exposed to ischemia and reperfusion for 20 min and 40 min, respectively. Cardiodynamic parameters including rate pressure product (RPP), heart rate (HR), the maximum up/down rate of left ventricular pressure (${\pm}dp/dt$), left ventricular developed pressure (LVDP), and coronary artery flow (CF) were achieved from Lab Chart software data. The Bax and BCl-2 gene expressions were measured in heart samples. Results: Hearts treated with TP extract and vit C represented a meaningful improvement in cardiac contractile function and CF. The overexpression of Bcl-2, downregulation of Bax, and improvement of apoptotic index (Bax/Bcl-2) were observed in pretreated TP extract and vit C hearts. Conclusion: The TP extract was found to ameliorate the cardiac function in the reperfused myocardium. Also, it can hinder apoptotic pathways causing cardioprotection.

• 한국임상수의학회지
• /
• 제26권3호
• /
• pp.200-204
• /
• 2009

This study was performed to evaluate the effects of reduced L-glutathione on the oxidant/antioxidant status(superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GPx), protein carbonyl and lipid hydroperoxide(LPO) concentration), renal function(blood urea nitrogen(BUN) and serum creatinine levels), and microscopy of renal tissues in pigs undergoing unilateral renal ischemia-reperfusion(I/R). Sixteen Landrace and Yorkshire mixed-breed pigs were divided randomly into two groups: untreated control group and reduced L-glutathione-treated group(4 mg/kg IV). Each group had 8 pigs. Pigs were unilaterally nephrectomized and the kidney was subject to 30 min of renal pedicle occlusion. Blood samples for biochemical assay were collected on days 1, 3, 5, 7, and 14 post nephrectomy. Renal I/R injury were evaluated histopathologically by the microscopic observation of renal tissue sections and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as SOD, GPx, CAT, protein carbonyl and LPO were measured. The elevation of creatine and BUN levels was lower in the treated group, compared with the control group. The activities of antioxidant-enzyme were higher in the treated group, compared with the control group. In histological findings, the severity of damage in the reduced L-glutathione treated group was less when compared to the control group.

• Nutrition Research and Practice
• /
• 제13권3호
• /
• pp.205-213
• /
• 2019

BACKGROUND/OBJECTIVES: Myocardial infarction (MI) is caused by extensive myocardial damage attributed to the occlusion of coronary arteries. Our previous study in a rat model of ischemia/reperfusion (I/R) demonstrated that administration of arabinoxylan (AX), comprising arabinose and xylose, protects against myocardial injury. In this study, we undertook to investigate whether psyllium seed husk (PSH), a safe dietary fiber containing a high level of AX (> 50%), also imparts protection against myocardial injury in the same rat model. MATERIALS/METHODS: Rats were fed diets supplemented with PSH (1, 10, or 100 mg/kg/d) for 3 d. The rats were then subjected to 30 min ischemia through ligation of the left anterior descending coronary artery, followed by 3 h reperfusion through release of the ligation. The hearts were harvested and cut into four slices. To assess infarct size (IS), an index representing heart damage, the slices were stained with 2,3,5-triphenyltetrazolium chloride (TTC). To elucidate underlying mechanisms, Western blotting was performed for the slices. RESULTS: Supplementation with 10 or 100 mg/kg/d of PSH significantly reduces the IS. PSH supplementation (100 mg/kg/d) tends to reduce caspase-3 generation and increase BCL-2/BAX ratio. PSH supplementation also upregulates the expression of nuclear factor erythroid 2-related factor 2 (NRF2), and its target genes including antioxidant enzymes such as glutathione S-transferase mu 2 (GSTM2) and superoxide dismutase 2 (SOD2). PSH supplementation upregulates some sirtuins ($NAD^+$-dependent deacetylases) including SIRT5 (a mitochondrial sirtuin) and SIRT6 and SIRT7 (nuclear sirtuins). Finally, PSH supplementation upregulates the expression of protein kinase A (PKA), and increases phosphorylated cAMP response element-binding protein (CREB) (pCREB), a target protein of PKA. CONCLUSIONS: The results from this study indicate that PSH consumption reduces myocardial I/R injury in rats by inhibiting the apoptotic cascades through modulation of gene expression of several genes located upstream of apoptosis. Therefore, we believe that PSH can be developed as a functional food that would be beneficial in the prevention of MI.

• 생물환경조절학회지
• /
• 제22권4호
• /
• pp.408-412
• /
• 2013

본 연구는 토마토 코이어 자루재배시 습해의 원인을 구명하고 습해를 방지하기 위하여 실시하였다. 실험은 미니찰을 고시하고 단동형 2중 플라스틱하우스에서 실시되었다. 배양액은 Yamazaki 토마토 전용배양액을 사용하였으며, 배양액 공급시간은 해뜨고 1시간 후 시작하여 해지기 2시간 전에 종료하였다. 자루당 I자형 찢기 및 L자형 찢기는 6개씩 15cm 길이로 찢었으며, 밑 찢기는 3개씩 15cm 길이로 뚫었다. 배액구 위치에 따른 배지무게는 포습 24시간 후 I자형 찢기는 14.2kg, L자형 찢기는 13.8kg, 밑 찢기는 12.8kg로 밑 찢기가 가장 가벼웠다. 포습 24시간 후 1일 관수하여 무게를 측정한 결과 I자형 찢기는 14.5kg, L자형 찢기 14.2kg, 밑 찢기 13.3kg로 역시 밑 찢기가 가벼웠다. 이것은 밑 찢기에서 배지내 함수량이 가장 적은 것을 의미한다. 부정근 발생정도는 I자형 뚫기 및 L자형 뚫기에서 160 및 170개 발생하였으나 밑 뚫기에서는 53개 발생하였다. 뿌리의 건물중(5주)은 밑 찢기가 57g으로 I자형 찢기 23g 및 L자형 찢기 25g과 비교해서 2배 이상 높았으며, 뿌리길이도 밑 찢기가 31.4cm로 다른 찢기 방법과 비교하여 길었다. 상품수량은 밑 찢기가 26.5kg/20주 로 I자형 찢기 19.7kg, L자형 찢기 24.0kg와 비교해 높은 수량성을 보였다. 따라서 U자형 베드에서 코이어 자루배지를 이용하여 수경재배를 할 경우 배액구는 밑 찢기로 만들어야 습해를 방지하여 생산성을 높일 수 있을 것으로 사료되었다.

• Journal of Chest Surgery
• /
• 제35권7호
• /
• pp.501-510
• /
• 2002

배경: 급성 호흡곤란증후군은 다양한 병인에 의해 발병하지만 그 병인론이 아직까지 확립되어 있지 않다. 본 연구에서는 장의 허혈-재관류시에 발병하는 급성 호흡곤란증후군에서 group II phospholipase $A_2$ ($PLA_2$)의 역할을 알아보기 위하여 시행되었다. 특히 폐장내의 호중구의 침윤과 더불어 유발되는 산화성 스트레스에서 group II $PLA_2$의 역할을 규명하려 하였다. 대상 및 방법: 체중 300g 내외의 Sprague-Dawley 종 흰쥐에서 급성 폐손상을 유발하기 위하여 상장간막동맥을 60분간 차단한 후 120분간 재관류를 시행하였다. Group II $PLA_2$가 폐장의 손상, 특히 혈관 내피세포의 손상에 미치는 영향을 호중구의 작용과 연관하여 알아보기 위하여 폐누출지수, 폐장내 myeloperoxidase의 활성도, 폐포세척액내의 단백함량을 측정하였다. 또한 장의 허혈-재관류에 따른 폐장내 $PLA_2$ 활성도의 변화를 검사하였고, 호중구에서의 산소기 형성에 미치는 group II $PLA_2$의 역할은 분리된 호중구에 rutin, manoalide, scalaradial과 같은 group II $PLA_2$ 억제제를 이용하여 산소기 생성이 억제됨을 확인함으로써 알아보았다. 장의 허혈-재관류에 따른 폐장 조직의 산화성 스트레스를 확인하기 위해 광학현미경법 및 cerium chloride를 이용한 세포화학적인 전자현미경법을 이용하여 폐장내 산소기의 생성을 확인하였다. 결과: 장의 허혈-재관류 후 폐장내 호중구의 침윤과 함께 급성 폐손상이 유발되었고, 폐장내 myeloperoxidase 활성도, 폐누출지수 및 폐세척액내의 단백함량이 대조군에 비해 유의하게 증가하였다(p<0.001). 폐장 및 장에서의 group II $PLA_2$ 활성도는 허혈-재관류 후 폐장, 장 모두에서 유의하게 증가하였고, rutin에 의해서 현저히 감소하였다(p<0.001). 사람의 혈액에서 분리된 호중구에서의 산소기 생성을 cytocrhome-c reduction assay를 통해 알아본 결과 rutin, manoalide, scalaradial 같은 group II PLA, 억제제에 의해 호중구의 산소기 생성이 감소함을 알 수 있었다. 허혈-재관류 후 광학현미경적 소견은 폐장내 염증세포의 침윤 및 모세혈관 주위의 부종이 관찰되었으나 rutin에 의해 이러한 변화는 억제되었다. $CeCl_3$을 이용한 세포화학적 전자현미경 실험에서 허혈-재관류 후 과산화수소의 생성이 증가하고 rutin에 의해서는 억제됨을 확인하였다. 결론: Croup II $PLA_2$의 억제는 침윤된 호중구로부터 산화기 생성을 억제함으로써 급성 폐손상을 완화하는 것으로 보이며, 따라서 group II $PLA_2$는 장 허혈-재관류로 유도된 급성 폐손상의 산화성 스트레스에서 중요한 역할을 하는 것으로 보인다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제3권6호
• /
• pp.579-586
• /
• 1999

Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement- dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg) to I/R hearts in the presence of PMNs $(100{\times}10^6)$ and homologous plasma improved coronary flow and preserved cardiac contractile function (p＜0.001) in comparison to those I/R hearts receiving only vehicle. In addition, C1 INH significantly (p＜0.001) reduced PMN accumulation in the ischemic myocardium as evidenced by an attenuation in myeloperoxidase activity. These findings demonstrate the C1 INH is a potent and effective cardioprotective agent inhibits leukocyte-endothelial interaction and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.

• 대한수의학회지
• /
• 제44권3호
• /
• pp.329-334
• /
• 2004

Ischemia/reperfusion(I/R) injury of the rat testis causes germ cell death and infiltration of inflammatory cells. To investigate the mechanism of germ cell death in torsion of the rat testis, apoptosis and macrophage activation were studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling(TUNEL) method and immunohistochemistry in the testes of Sprague-Dawley rats subjected to 1.5 h of ischemia, followed by 0, 1, 3, 6, 12, 24, 48 and 96 h of reperfusion. Apoptotic, TUNEL-positive cells were found at the base of the seminiferous epithelia after I/R. TUNEL-positive cells were significantly increased 6 h after repair of the torsion, and there was a significant peak in apoptosis 24 h after reperfusion, as compared with normal or sham-operated controls. In contrast, histological evidence of germ cell necrosis in the seminiferous tubules was first visible 24 h after reperfusion. In the testis of sham-operated rats, ED2-positive resident macrophages were found diffusely in the interstitial space, while ED1-positive monocyte-like macrophages were rarely found. After I/R, ED1-positive cells were significantly increased beginning 12 h after reperfusion, while ED2-positive immunoreactivity did not change during the experimental period. Together, the results of this study confirmed that increased numbers of ED1-positive macrophages, but not resident ED2-positive macrophages, infiltrated the interstitial space surrounding damaged tubules and induced germcell death.

• 대한화장품학회:학술대회논문집
• /
• 대한화장품학회 2003년도 IFSCC Conference Proceeding Book I
• /
• pp.601-610
• /
• 2003

Biotin is a water-soluble vitamin used as a skin conditioning agent and promotes the formation of intercellular lipid layers through increased lipid synthesis, which improves the skin's natural barrier function. The anti-inflammatory effects of biotin have been investigated using in vitro assay models, such as MTT assay, measurements of concentrations of nitric oxide(NO), prostaglandin E2(PGE$_2$), and inhibition rate of 5-lipoxygenase(5-LOX). In comparison with biotin, other plant extracts were tested at the same time which were kudzu vine extract, sage extract, paeonia extract, and dipotassium glycyrrhetinate. Nitric oxide is a signal molecule with functions such as neurotransmission, local vascular relaxation, and anti-inflammation in many physiological and pathological processes. NO can cause apoptosis and necrosis of target cells such as keratinocytes and is generated from L-arginine by nitric oxide synthase (NOS). Prostanoids, including prostaglandins and thromboxanes, are generated by the phospholipase $A_2$/cyclooxygenase(COX) pathway, and leukotrienes are generated by the 5-lipoxygenase pathway from arachidonic acid. Prostaglandin E2 recently have been shown to be beneficial in the resolution of tissue injury and inflammation, also has been implicated as an immunosuppressive agent and plasma levels of PGE$_2$ are elevated in patients sustaining thermal injury. Lipoxygenase metabolites from arachidonic acid have been implicated in inflammation, anti-inflammatory activity of the raw materials was evaluated in vitro by the offered inhibition of lipoxygenase.

• Biomolecules & Therapeutics
• /
• 제25권4호
• /
• pp.383-389
• /
• 2017

Dexmedetomidine is an ${\alpha}2$-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of $1{\mu}g/kg$ load dose, followed by $0.05{\mu}g/kg/min$ infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-$1{\beta}$, interleukin-6 and tumor nevrosis factor-${\alpha}$ as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-${\kappa}Bp65$, inhibitor of ${\kappa}B{\alpha}$ and phosphorylated of ${\kappa}B{\alpha}$ in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-${\kappa}B$ pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.