Estrogen and ghrelin decrease cytoplasmic expression of p27<Superscript>kip1</Superscript>, a cellular marker of ageing,in the striated anal sphincter and levator muscle of ovariectomized rats

A study was carried out to investigate the effect of estrogen and/or ghrelin on the cellular marker of ageing, p27^kip1, in pelvic floor muscles of ovariectomized rats. Virgin Wistar rats (13 months old) underwent ovariectomy followed (1 month) by 42 daily intraperitoneal 17-β estradiol (10 μg/kg), ghrelin (2 μg/kg), both hormones, or placebo vehicle (n=6×4 groups). Six more age-matched animals underwent sham surgery without ovariectomy. Cytoplasmic expression of p27^kip1 in the striated urethral and anal sphincters and levator muscle was measured by Western blot analysis in all animals (n=30). p27^kip1 signal intensity significantly increased postovariectomy in all muscles compared to sham animals. In the anal sphincter and levator, signal intensity decreased to sham levels with ghrelin or estrogen and decreased further after estrogen or ghrelin and estrogen/ghrelin administration. Urethral sphincter signal intensity decreased without reaching sham levels after drug administration. Estrogen and/or ghrelin replacement reverses the ovariectomy-induced exacerbation of biochemical cellular ageing in the anal sphincter and levator muscle of middle-aged rats.     

Combined estrogen and ghrelin administration restores number of blood vessels and collagen type I/III ratio in the urethral and anal canal submucosa of old ovariectomized rats

We compare the effects of estrogen and/or ghrelin on vascular counts and collagen I/III ratio of urethral and anal canal submucosa in old vs young-adult ovariectomized rats. Ovariectomized Fisher 344 rats (18 and 3 months old, n = 24 x 2) received 42 daily intraperitoneal 17-ss estradiol (10 microg/kg), ghrelin (2 microg/kg), both, or vehicle (n = 6 x 4 per group). Blood vessel counts and collagen I/III ratio were measured, respectively, by light microscopy and Western blot analysis with immunohistochemistry of ghrelin receptors. Estrogen significantly increased urethral and anal vascular counts and collagen I/III ratio in young-adult rats. In old rats, only combined estrogen/ghrelin administration significantly increased both variables. This was not observed with estrogen or ghrelin separately. Ghrelin receptors were immunostained in urethral and anal submucosa of all samples. Combined estrogen/ghrelin administration restored postovariectomy urethral and anal canal submucosal vessel number and collagen I/III ratio in old rats suggesting independent ageing effect.     

重组人甲状旁腺素（1-34)与雌激素对去卵巢大鼠骨代谢的影响

目的观察重组人甲状旁腺素(1-34)与雌激素单用和联用对去卵巢大鼠骨代谢的影响。方法选用雌性4月龄SD大鼠45只,随机分为5组:①假手术(Sham)8只;②去卵巢(OVX)9只;③雌激素治疗组(OVX E)10只:OVX2个月后给予苯甲酸雌二醇治疗6w;④PTH治疗组(OVX PTH)9只:OVX2个月后给予rhPTH(1-34)治疗6w;⑤雌激素与PTH联合治疗组(OVX E PTH)9只:OVX2个月后给予rhPTH(1-34)和E2联合治疗6w。观察各组大鼠胫骨近端松质骨骨小梁形态计量学参数,椎体生物力学指标及部分血清骨生化代谢指标。结果雌激素治疗组和PTH治疗组的骨静态参数均表现为骨量增加;雌激素治疗组的骨形成参数和骨吸收参数降低;PTH治疗组的骨形成指标明显升高,而骨吸收指标虽较Sham高,但较OVX组有所降低;E2与PTH联合治疗组与单用E2组和单用PTH组比较,骨量明显提高,骨转换率参数介于单用E2和单用PTH组之间。3个治疗组的生物力学指标较OVX组均有明显提高,其中E2与PTH联合治疗组改善最明显。结论雌激素和PTH可使去卵巢大鼠松质骨骨量增加和改善生物力学性能,两者联合治疗有协同作用。     

Estrogen downregulates the proximal tubule type IIa sodium phosphate cotransporter causing phosphate wasting and hypophosphatemia

Estrogen treatment causes significant hypophosphatemia in patients. To determine the mechanisms responsible for this effect, we injected ovariectomized rats with either 17beta-estradiol or vehicle for three days. Significant renal phosphate wasting and hypophosphatemia occurred in estrogen-treated rats despite a decrease in their food intake. The mRNA and protein levels of the renal proximal tubule sodium phosphate cotransporter (NaPi-IIa) were significantly decreased in estradiol-treated ad-libitum or pair-fed groups. Estrogen did not affect NaPi-III or NaPi-IIc expression. In ovariectomized and parathyroidectomized rats, 17beta-estradiol caused a significant decrease in NaPi-IIa mRNA and protein expression compared to vehicle. Estrogen receptor alpha isoform blocker significantly blunted the anorexic effect of 17beta-estradiol but did not affect the downregulation of NaPi-IIa. Our studies show that renal phosphate wasting and hypophosphatemia induced by estrogen are secondary to downregulation of NaPi-IIa in the proximal tubule. These effects are independent of food intake or parathyroid hormone levels and likely not mediated through the activation of estrogen receptor alpha subtype.     

重组人生长激素对摘除卵巢大鼠皮质骨的影响

目的 探讨重组人生长激素对摘除卵巢大鼠股骨和椎体皮质骨的影响。方法 ６个月龄ＳＤ大鼠４０只,摘除卵巢后３个月开始皮下注射高、低２种剂量生长激素。注射８周后处死,取出双侧股骨和Ｌ２椎体,测定股骨中段骨密度值,观测股骨中段和椎体皮质骨厚度的改变,测定股骨生物力学强度,并与雌激素注射组比较。结果 生长激素显著增加摘除卵巢大鼠股骨中段和腰椎体皮质骨尤其是外层皮质的厚度,股骨中段骨密度值和生物力学强度出显著     

Chemically modified tetracycline (CMT-8) and estrogen promote wound healing in ovariectomized rats: Effects on matrix metalloproteinase-2, membrane type 1 matrix metalloproteinase, and laminin-5 γ2-chain

Estrogen deficiency is associated with impaired cutaneous wound healing. Remodeling of the extracellular matrix in wound healing involves the action of matrix metalloproteinases on basement membrane zone components, especially laminin-5. We studied the effects of estrogen and a potent matrix metalloproteinase inhibitor, chemically modified non-antimicrobial tetracycline, CMT-8, on wound healing in ovariectomized rats. At the tissue level, laminin-5 gamma2-chain expression was decreased and the migration-inductive 80 kDa form of laminin-5 gamma2-chain was absent in ovariectomized rats when compared with sham and CMT-8- or estrogen-treated ovariectomized animals as detected by Western blotting. The highest levels of gelatinolytic activity (matrix metalloproteinase-2 and -9) were found in sham animals. Levels were reduced in ovariectomized rats and were lowest after treating ovariectomized rats with CMT-8 or estrogen as analyzed by functional activity assay and zymography. The total amount of membrane type 1-matrix metalloproteinase was unchanged in all groups. We conclude that CMT-8 and estrogen can promote wound healing in ovariectomized rats, not only by normalizing wound bed total collagen content and structure, but also by recovering the expression and processing of key molecules in wound healing, i.e., laminin-5 gamma2-chain. This study shows, for the first time, the role of estrogen and CMT-8 in laminin-5 gamma2-chain modulation in vivo.     

Tamoxifen prevents the skeletal effects of ovarian hormone deficiency in rats

To determine whether the nonsteroidal antiestrogen tamoxifen behaves as either an agonist or antagonist of estrogen on bone, the effects of ovariectomy, 17 beta-estradiol, and tamoxifen were compared on radial growth at the tibial diaphysis in young adult female rats. Ovariectomy and 17 beta-estradiol did not alter serum calcium, phosphate, or 25-hydroxyvitamin D. Ovariectomy increased serum 1,25-dihydroxyvitamin D in one experiment but not in the other. Tamoxifen increased the serum calcium and phosphate by itself and did not change serum 1,25-dihydroxyvitamin D in ovariectomized rats. Ovariectomy produced significant increases in medullary area, periosteal bone formation rate, and periosteal bone apposition rate compared to values in sham-operated animals and did not change endosteal bone formation rate. The increase in medullary area resulted from an increase in osteoclast number and resorbing surface length. Although endosteal forming surface length decreased, this was compensated for by an increase in the apposition rate. 17 beta-estradiol and tamoxifen each prevented the increases in bone formation rate and medullary area in ovariectomized rats. Tamoxifen reduced the length of the resorbing surface and osteoclast number to values observed in sham-operated animals. The findings demonstrate that in the rat, tamoxifen acts as an estrogen agonist by preventing the skeletal alterations that result from ovarian hormone deficiency.     

Estrogen and progesterone regulate alpha, beta, and gammaENaC subunit mRNA levels in female rat kidney

BACKGROUND: Estrogen and progesterone regulate alpha, beta, and gamma amiloride-sensitive epithelial sodium channel (ENaC) subunit mRNA levels in female rat kidney. Renal Na(+) handling differs between males and females. Further, within females Na(+) metabolism changes during the menstrual cycle and pregnancy. Electrolyte homeostasis and extracellular fluid volume are maintained primarily by regulated transport of Na(+) via the amiloride-sensitive Na(+) channel. This study examines the role of the female gender steroids in the regulation of expression of ENaC. METHODS: We measured ENaC subunit mRNA levels in rat kidney using Northern blotting. Kidneys were taken from male and females at different ages and from adult ovariectomized rats treated with 17-beta-estradiol benzoate (estrogen) and/or progesterone for 8 or 24 hours. RESULTS: The abundance of alpha, beta, and gammaENaC mRNA was significantly higher in female compared to male rat kidneys from 10 weeks of age (P= 0.001, P= 0.004, and P= 0.02, N= 10, respectively). These differences were abolished in ovariectomized rats. Treatment of ovariectomized rats with estrogen increased alphaENaC mRNA abundance in the kidney at both 8 and 24 hours (P < 0.05, N= 6; and P < 0.05, N= 7, respectively). Progesterone inhibited the effect of estrogen on alphaENaC mRNA at 8 hours but when given alone increased gammaENaC mRNA (P < 0.05, N= 3). Neither hormone, alone or in combination, had any significant effect on betaENaC mRNA levels at 8 or 24 hours. CONCLUSION: Female gonadal steroids differentially modulate expression of ENaC subunit mRNA in the rat kidney.     

Effect of ovariectomy on dexamethasone- and progesterone-dependent osteoprogenitors in vertebral and femoral rat bone cell populations

We have found previously that the skeleton of adult female rats contains dexamethasone (Dex)- and progesterone (Prog)-dependent osteoprogenitors, and that estrogen treatment in vitro upregulates proliferation and differentiation of the Prog-dependent but not of the Dex-dependent osteoprogenitors (Bone 1997;20:17-25). The purpose of the present study was to determine whether ovariectomy (OVX) would have different effects on these two classes of osteoprogenitors. Six-month-old Sprague-Dawley rats underwent OVX and the lumbar vertebrae and proximal femurs were collected 1.5, 3, and 6 months after OVX. Cells were obtained from outgrowths of explant cultures and grown in alpha-MEM with 10% FBS, 50 microg/ml ascorbic acid, and 5 mM beta-glycerophosphate. Osteoprogenitors were identified by their ability to generate a colony of osteoblastic cells forming bone (bone nodule). We also evaluated the number of colony-forming units-fibroblast (CFU-F) and of alkaline phosphatase (AP)-positive CFU-F. In cell populations obtained from vertebrae of rats ovariectomized for 1.5, 3, and 6 months and their corresponding control rats, both Dex (1-100 nM) and Prog (1-10 microM) dose-dependently stimulated nodule formation. Both Dex- and Prog-induced nodule formation were higher in cell populations from control rats than in those from ovariectomized rats (P < 0.001). Numbers of CFU-F and AP-positive CFU-F were also higher in cell populations from control rats compared with those from ovariectomized rats. Estrogen (10 nM) enhanced Prog-dependent bone nodule formation but decreased Dex-dependent bone nodule formation in populations from both control and ovariectomized rats. In femoral populations, the responses to Dex (10 nM), Prog (3 microM), and estrogen (10 nM) were similar to those of the vertebral populations in both control and ovariectomized rats. Our results demonstrate that ovariectomy in rats results in a dramatic decrease in the number of both Dex- and Prog-dependent osteoprogenitors in cell populations from vertebrae and proximal femurs. In addition, we confirmed our previous observation that estrogen upregulated proliferation and differentiation of Prog-dependent progenitors, but found here that estrogen clearly downregulated proliferation and differentiation of the Dex-dependent progenitors.     

Cellular and molecular mechanisms regulating vascular tone. Part 2: regulatory mechanisms modulating Ca<Superscript>2+</Superscript> mobilization and/or myofilament Ca<Superscript>2+</Superscript> sensitivity in vascular smooth muscle cells

Understanding the physiological mechanisms regulating vascular tone would lead to better circulatory management during general anesthesia. This two-part review provides an overview of current knowledge about the cellular and molecular mechanisms regulating the contractile state of vascular smooth muscle cells (i.e., vascular tone). The first part reviews basic mechanisms controlling the cytosolic Ca²⁺ concentration in vascular smooth muscle cells, and the Ca²⁺-dependent regulation of vascular tone. This second part reviews the regulatory mechanisms modulating Ca²⁺ mobilization and/or myofilament Ca²⁺ sensitivity in vascular smooth muscle cells—including Rho/Rho kinase, protein kinase C, arachidonic acid, Ca²⁺/calmodulin-dependent protein kinase II, caldesmon, calponin, mitogen-activated protein kinases, tyrosine kinases, cyclic nucleotides, Cl⁻ channels, and K⁺ channels.     

Regulation of growth hormone secretagogue receptor gene expression in the arcuate nuclei of the rat by leptin and ghrelin

The anorexigenic and orexigenic hormones leptin and ghrelin act in opposition to one another. When leptin signaling is reduced, as in the Zucker fatty rat, or when circulating ghrelin is increased during fasting, the effect of ghrelin becomes more dominant, indicating an influence of both hormones on ghrelin action. This effect could be mediated via the level of expression of ghrelin receptor (growth hormone secretagogue receptor [GHS-R]). For testing this, GHS-R expression was measured using in situ hybridization in Zucker fatty versus lean rats; in fed versus fasted (48 h) rats, treated with either ghrelin or leptin; and in GH-deficient, dwarf versus control rats. In the arcuate nuclei of the Zucker fatty rat and in fasted rats, GHS-R expression is significantly increased. A single leptin intracerebroventricular injection attenuated the fasting-induced increase in GHS-R but had no effect in fed rats 2 h after injection, whereas leptin infusion for 24 h or longer significantly decreased GHS-R expression in fed rats. Ghrelin significantly increased GHS-R expression but not in dwarf rats. These results show that the level of GHS-R expression in the ARC is reduced by leptin and increased by ghrelin and that the effect of ghrelin may be GH dependent.     

Estrogen and postnatal maturation increase caveolar number and caveolin-1 protein in bladder smooth muscle cells

PURPOSE: Clinical studies indicate that detrusor contractility decreases in old age and the dense band pattern with caveolar depletion represents the ultrastructural norm of the aged human detrusor. We performed animal studies to explore the hypothesis that lowering estrogen induces the dense band pattern with estrogen replacement restoring usual sarcolemmal appearance and increasing caveolar number. MATERIALS AND METHODS: Newborn, young (1-month-old) and middle-aged (13 to 14-month-old) female rats were studied. Middle-aged animals were evaluated 4 months after sham operation or ovariectomy (OVx) with OVx rats receiving placebo or 25% 17beta-estradiol (E2) capsules for 1 week prior to sacrifice. Electron microscopy was used to evaluate sarcolemmal structure and quantify caveolar numbers in bladder muscle cells. Caveolae were also assessed by measuring caveolin-1 protein. RESULTS: Alternating electron dense and thinner zones with abundant caveolae were present in bladder sarcolemma from middle-aged animals. Newborn and OVx sarcolemma showed many ultrastructural features of the dense band pattern with fewer caveolae present per micro sarcolemma or per muscle cell compared with sham operated middle-aged controls. E2 replacement decreased the dense band pattern and increased caveolar numbers in OVx animals. Caveolin-1 protein levels underwent similar changes following maturation, OVx and E2 replacement, while alpha-smooth muscle actin remained unchanged. CONCLUSIONS: Prolonged estrogen withdrawal results in sarcolemmal changes in middle-aged animals, similar to the dense pattern observed in newborns. Estrogen replacement decreases the dense pattern, while increasing caveolar numbers and caveolin-1 protein. It remains to be seen whether estrogen influences caveolar depletion and/or contractility in human bladders.     

Age Dependent Repair of Muscle Rupture: A Histological and Microangiographical Study in Rats

Healing of contusion injury in the gastrocnemius muscle was studied in young adult and old rats. A standard blunt muscle contusion was induced to the left calf of each animal and studied histologically and microangiographically 2-21 days after the injury. The inflammatory cell reaction was more intense, the haematoma was larger and the proliferation of fibroblasts and production of collagen scar more pronounced in the young rats. The sprouting of new capillaries and regeneration of ruptured muscle fibres occurred more rapidly and intensively in the young animals, and the resorption of haematoma and phagocytosis of necrotic tissue occurred later in the old rats.

The decreased repairing capacity in muscles of older animals resembles that seen earlier in immobilized muscles of adult rats, indicating that the response to the stimulus of injury decreases with advancing age.     

The rat arcuate nucleus integrates peripheral signals provided by leptin,insulin, and a ghrelin mimetic

The hypothalamic circuits controlling food intake and body weight receive and integrate information from circulating satiety signals such as leptin and insulin and also from ghrelin, the only known circulating hormone that stimulates appetite following systemic injection. Activation of arcuate neurons by ghrelin and ghrelin mimetics (the growth hormone secretagogues) is augmented in 48-h-fasted rats compared with fed rats, as reflected by a greater number of cells expressing Fos protein in response to administration of the same maximally effective dose. Here we sought to determine whether this increased responsiveness in fasting might reflect or be influenced by low levels of circulating satiety factors such as leptin or insulin. Chronic central infusion of insulin or leptin during a 48-h fast suppressed the threefold increase in the Fos response to intravenous injection of a maximally effective dose of growth hormone-releasing peptide (GHRP)-6, a synthetic growth hormone secretagogue. This appears to be a direct central action of insulin and leptin because the marked decrease in plasma levels of insulin, leptin, and glucose during fasting were unaffected by central administration of either hormone. Furthermore, the GHRP-6-induced Fos response was twofold greater in obese leptin- and insulin-resistant Zucker rats compared with lean controls. These data provide evidence that the ghrelin-sensitive circuits in the hypothalamus are dynamically regulated by central insulin and leptin action.     

Long-term observation of the detrusor smooth muscle in rats

Summary We studied the bladders of 24-month-old intact rats, rats that had been ovariectomized at the age of 6 months, and intact and ovariectomized rats treated by estrogen from the age of 16 months. The study thus comprized four groups: group I: bilaterally ovariectomized rats; group II: intact rats; group III: ovariectomized rats treated with estrogen; group IV: intact rats treated with estrogen. The weight and collagen concentration of the bladders were determined. The ovariectomized bladders weighed significantly less and had a higher collagen concentration than the intact bladders. Estrogen substitution for ovariectomized rats reversed these parameters. Detrusor strips were also used for organ bath studies. All bladders were similar in regard to the nervemediated frequency-response relationship. The atropine-resistant response was studied by adding scopolamine to the organ bath. Strips from ovariectomized rats had a significantly diminished atropine-resistant response, which was abolished by estrogen substitution. The present study suggests that micturition problems in menopause might have a structural as well as a pharmacological explanation.     

Different Effects of Estrogen and Progesterone on K+ Currents Expressed in Xenopus Oocytes

Estrogen has received considerable attention recently as a potential therapeutic agent in vascular pathophysiological states such as stroke. The mechanisms by which estrogen influences cerebral arteries are incompletely understood. The present study was to examine the effect of ovariectomy and chronic estrogen or tamoxifen treatment on vascular reactivity in rat posterior communicating cerebral arteries with intact endothelium. Changes in vascular tension were measured by microvessel myograph. Ovariectomy significantly enhanced the constricting responses to endothelin I, but not to phenylephrine. Chronic treatment with estrogen or tamoxifen partially reversed or abolished the effect of ovariectomy. The contraction induced by high K⁺ solution was also enhanced in the ovariectomized rats and this enhancement was abolished by estrogen or tamoxifen treatment. Ovariectomy potentiated the relaxant response to nicardipine but not NS 1619. Estrogen but not tamoxifen reversed the effect of ovariectomy. The present results indicate that chronic tamoxifen may not act as an antagonist of estrogen, instead, chronic treatment with estrogen and tamoxifen has similar effect in inhibiting the increased vascular tension induced by ovariectomy. This study suggests the influence of physiological level of estrogen on vascular contractility. It is at present unknown what may have caused increased relaxant effect of nicardipine, a L-type Ca²⁺ channel blocker. More experiments are needed to show the role of endothelium in the altered vascular contractility in the ovariectomized and estrogen-treated rats. (supported by UPGC Direct Grant).     

Estrogen alone or in combination with parathyroid hormone can decrease vertebral MEF2 and sclerostin expression and increase vertebral bone mass in ovariectomized rats

Summary

The study is about the regulatory effects of estrogen and parathyroid hormone (PTH) on sclerostin, a protein that inhibits the Wnt/β-catenin pathway. The results indicate that estrogen may down-regulate sclerostin expression and that estrogen displays synergistic action with PTH. These results provide a new perspective on the relationship between estrogen and bone.

Purpose

To investigate whether estrogen can down-regulate SOST and MEF2 (myocyte enhancer factor 2) expression and whether co-treatment with estrogen and PTH has a stronger effect on suppressing SOST than PTH applied alone in ovariectomized rats.

Methods

Forty-three-month-old virgin female Sprague–Dawley (SD) rats were ovariectomized and divided into four groups (n?=?10). Another ten age-matched rats received sham operations as controls. After allowing 8 weeks for the development of vertebral osteopenia, the rats were administered the drug intervention. For this intervention, the estrogen group was subcutaneously injected with 17β-estradiol at 25 μg/kg body weight, the PTH group was injected with 80 μg/kg synthetic human PTH (1–34), and the co-treatment group was concurrently treated with PTH and estrogen at the above dosage. The OVX group and sham group were treated with vehicle. The drug treatment was conducted for 12 weeks. After the lumbar spine bone mineral density (BMD) was measured, the rats were sacrificed, and the lumbar spine and blood were collected for qPCR, Western blot, immunohistochemistry and other tests.

Results

Estrogen can down-regulate MEF2 and sclerostin expression, and co-treatment with estrogen and PTH has a stronger effect on suppressing MEF2 and SOST mRNA than PTH alone. The co-treatment group displayed slightly higher bone mass and biomechanical properties than the PTH group, but the differences were not significant.

Conclusions

Estrogen appears to be a regulator of sclerostin, and the effect may involve suppressing MEF2s. Combined treatment with PTH and estrogen is not more beneficial for vertebral bone mass and strength than treatment with PTH alone in ovariectomized rats.     

Cortical bone mass,composition, and mechanical properties in female rats in relation to age,long-term ovariectomy,and estrogen substitution

Summary The study comprised 12 groups of female rats: 6 groups of intact rats killed at 2, 6, 9, 12, 15, and 24 months of age, 4 groups of rats ovariectomized at 6 months and killed together with the intact rats at 9, 12, 15, and 24 months of age, and 2 groups of rats (one intact and one ovariectomized) treated with estrogen (2 g estradiol valerate/rat/week s.c.) for 8 months before they were killed at 24 months of age. The composition, dimensions, and mechanical strength of intact bone and bone collagen from femoral diaphyses were investigated in relation to age, ovariectomy, and estrogen administration. Up to 6–9 months of age, the axial length, percentage ash, density, and compressive mechanical stress increased, whereas percentage collagen decreased. An age-related increase in bone mass, crosssectional area, and wall thickness and a decrease in mechanical quality of bone collagen were apparent from 2 to 24 months of age. An age-related periosteal bone formation and the absence of endosteal bone resorption were demonstrated in intact rats. Compared with intact rats, ovariectomy was followed by an increase in body weight, a tendency to reduced percentage ash and a depressed bone mass, crosssectional area, and wall thickness of femoral diaphyses. The compressive mechanical stress of intact bone and the mechanical quality of bone collagen were unaffected by ovariectomy. Ovariectomy did not influence the periosteal bone formation but induced an endosteal bone resorption not present in the intact rats. The estrogen treatment of the ovariectomized rats normalized the body weight of the rats and brought to an end the endosteal bone resorption induced by ovariectomy. Estrogen treatment of both ovariectomized and intact rats tended to reduced the rate of periosteal bone formation.     

不同水平大鼠脊髓损伤后盆底肌肉张力及神经肽的变化

目的 通过对脊髓损伤(SCI)后盆底肌肉张力和神经肽水平的观察,为SCI盆底功能障碍的机制研究和临床治疗提供依据.方法 SD雌性成年大鼠30只,随机分为骶髓上脊髓损伤组(SS)、骶髓下脊髓损伤组(SC)和正常对照组,每组各10只,采用脊髓离断法造模,4周后观察耻尾肌在体肌张力(顺应性和电刺激后的收缩活力)和神经肽变化.结果 SC组、SS组和正常组盆底肌肉顺应性分别为(16.23±4.46)g、(13.44±4.15)g和(14.46±5.61)g,SC组和SS组较正常组差异无统计学意义(P>0.05);SC组、SS组和正常组的最适初长度下收缩活力依次为(0.35±0.19)g、(2.80±2.12)g、(7.75±2.98)g,拉长后收缩活力依次为(2.61±0.73)g、(4.67±1.16)g、(14.86±3.79)g,SC组和SS组的收缩活力均明显低于正常组(P<0.05),且SC组较SS组更低(P<0.05);SC组和Ss组神经肽Y和血管活性肠肽含量均显著低于正常组(P<0.05),且SC组更低于SS组(P<0.05).结论 骶髓上和骶髓下水平脊髓损伤后盆底肌肉的收缩活力和神经肽水平显著下降,且骶髓下脊髓损伤后下降更加明显.脊髓损伤后盆底肌肉的异常变化值得重视.