| Pregnancy induced hypertension (PIH) may play a major role on the diseases occurrence and development in the world. It is one of the most common factors to cause infants and women death. At present, states of hypertension resulted in change of cell factors of the body and renal. Renal damage was one of the most characters of forerunner in PIH. Furthermore, Molecular mechanism of renal damage in PIH was is unknown in the world. Up to now, all world researchers paid important attention to intracellular signal transduction related with extracellular stimulate and regulation function. During the process of PIH, all kinds of active substance and growth factor acted on special receptors, produced transcript factor on intracellular signal transduction, incited special intracellular gene expression and promote biological effect.The term protein kinase C ( PKC ) stands for a group of at least twelve ser-ine/threconine kinase that are characterized by a high degree of similarity in their catalytic kinase domains and cysteine-rich regions. The PKC family is subdivided into three groups; the classical PKC members are Ca2 * and dia-cylglycerol dependent, the novel PKCn are Ca2+ -independent but dia-cylglycerol dependent and the atypical PKCs are not activated by Ca2+ and diacylglycerol in vitro. This may account for the multiplicity and diversity of the cellular activities implicated to be mediated by PKC, since individual PKC enzymes are thought to execute distince cellular functions, at different cellular locations. PKC isoenzymes exhibit distinct tissue distibution and play a critical role in the renal. Mitogen-activated protein kinase (MAPK) is one of the mostcommon serine/threconine kinase in the body of vertebrate animals. MAPK had three members-ERK, P38 and JNK. Recently there was a new member-ERKs. MAPK is common passage of intracellular messenger transduction to promote cellular proliferatian and key to enzyme of cell phenotype change and proliferation. As upper reaches signal molecule, PKC can active MAPK. Up to now it was not specially clinical drugs to cure renal damage.Low molecular weight heparin ( LMWH) extract from common heparin which was lack to choice and has side effect. In order to study molecular mechanisms of renal damage of PIH and intracellular signal transduction of LMWH, In order to build and improve the animal model of a stable PIH, we studied the effect of protein expression of PKC and MAPK in PIH. Through LMWH cure and prevention, renal damage of PIH can relieve and protect renal cells from injury induced by hypertension. We evaluated the protective effect of LMWH on nephropathy in PIH rats and explored its possible mechanism.Materials and Methods1. Trial animal; Wistar rats, weight 200-220g, week-age 14-16 weeks, pro- vided by CML trial animal department.2. Animal model; Female and male ( 1 ;2) match in the cage which environ- ment calm and warm and temperature 15 25. Secretion of female in the vagina was taken in the morning.3. Trial animal group; Pregnant rats were signed to four groups; normal control rats, normal pregnant rats, PIH rats and diabetic rats treated with LMWH. Each group were recorded to blood pressure in tail artery and average artery pressesure every day. When we begin to the medicine, urine protein was measured in urine volume of 24 hour the every two day.4. Specimen collections and laboratory check; In the 21 days of pregnant rats,infants were taken which registered weight and height after aesthesia. Cr and BUN in the blood were measured. And infants took a part of left kidney to soak into 10% formaldehyde liquid fixed with HE and PAS immunohistochemis-try. Another parts of kidneys were sheared roughly pieces (Imm3/piece) , andflushed with NS, conserving to -705. Determination of PKC and MAPK activity: For PKC activity assay, we use histone HI as substract for 7 minutes at 30 in a total reaction volume of 50ul. Induing 20mmol/L Tris/HCl, pH 7.5, 5mmol/L Mg( AC)2, 0. 5mmol/ L CaCl2, 2ug PS, 40ng DG, 0.01mmol ATP and 0.5...
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