共查询到20条相似文献,搜索用时 31 毫秒
1.
Hydrogen sulfide (H 2S) is a novel gasotransmitter that plays multiple biological roles in various body systems. In addition to its endogenous production, H 2S is produced by bacteria colonizing digestive organs, including the oral cavity. H 2S was previously shown to enhance pro-apoptotic effects in cancer cell lines, although the mechanisms involved remain unclear. To properly assess the anti-cancer effects of H 2S, however, investigations of apoptotic effects in normal cells are also necessary. The aims of this study were (1) to compare the susceptibility to H 2S-induced apoptosis between the oral cancer cell line Ca9-22 and oral keratinocytes that were derived from healthy gingiva, and (2) to identify candidate genes involved in the induction of apoptosis by H 2S. The susceptibility to H 2S-induced apoptosis in Ca9-22 cells was significantly higher than that in keratinocytes. H 2S exposure in Ca9-22 cells, but not keratinocytes, enhanced the expression of pleckstrin homology-like domain, family A, member 1 (PHLDA1), which was identified through a differential display method. In addition, PHLDA1 expression increased during actinomycin D-induced apoptosis in Ca9-22 cells. Knockdown of PHLDA1 expression by small interfering RNA in Ca9-22 cells led to expression of active caspase 3, thus indicating apoptosis induction. The tongue cancer cell line SCC-25, which expresses PHLDA1 at a high level, showed similar effects. Our data indicate that H 2S is an anti-cancer compound that may contribute to the low incidence of oral cancer. Furthermore, we demonstrated the role of PHLDA1 as an apoptosis suppressor. 相似文献
3.
Many studies have shown that hydrogen sulfide (H 2S) is both detrimental and beneficial to animals and plants, whereas its effect on bacteria is not fully understood. Here, we report that H 2S, released by sodium hydrosulfide (NaHS), significantly inhibits the growth of Escherichia coli in a dose-dependent manner. Further studies have shown that H 2S treatment stimulates the production of reactive oxygen species (ROS) and decreases glutathione (GSH) levels in E. coli, resulting in lipid peroxidation and DNA damage. H 2S also inhibits the antioxidative enzyme activities of superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) and induces the response of the SoxRS and OxyR regulons in E. coli. Moreover, pretreatment with the antioxidant ascorbic acid (AsA) could effectively prevent H 2S-induced toxicity in E. coli. Taken together, our results indicate that H 2S exhibits an antibacterial effect on E. coli through oxidative damage and suggest a possible application for H 2S in water and food processing. 相似文献
4.
Background Hydrogen sulphide (H 2S) is a gaseous neuro-mediator that exerts analgesic effects in rodent models of visceral pain by activating K ATP channels. A body of evidence support the notion that K ATP channels interact with endogenous opioids. Whether H 2S-induced analgesia involves opioid receptors is unknown. Methods The perception of painful sensation induced by colorectal distension (CRD) in conscious rats was measured by assessing the abdominal withdrawal reflex. The contribution of opioid receptors to H 2S-induced analgesia was investigated by administering rats with selective μ, κ and δ opioid receptor antagonists and antisenses. To investigate whether H 2S causes μ opioid receptor (MOR) transactivation, the neuronal like cells SKNMCs were challenged with H 2S in the presence of MOR agonist (DAMGO) or antagonist (CTAP). MOR activation and phosphorylation, its association to β arrestin and internalization were measured. Results H 2S exerted a potent analgesic effects on CRD-induced pain. H 2S-induced analgesia required the activation of the opioid system. By pharmacological and molecular analyses, a robust inhibition of H 2S-induced analgesia was observed in response to central administration of CTAP and MOR antisense, while κ and δ receptors were less involved. H 2S caused MOR transactivation and internalization in SKNMCs by a mechanism that required AKT phosphorylation. MOR transactivation was inhibited by LY294002, a PI3K inhibitor, and glibenclamide, a K ATP channels blocker. Conclusions This study provides pharmacological and molecular evidence that antinociception exerted by H 2S in a rodent model of visceral pain is modulated by the transactivation of MOR. This observation provides support for development of new pharmacological approaches to visceral pain. 相似文献
5.
Spinach plunts ( Spinacia oleracea L. cv. Monosa) were exposed to air with and without 0.25 μl l -1 H 2S. Effects of H 2S exposure for up to 18 days on photosynthesis, dark respiration and on chlorophyll a fluorescence were studied. Dark respiration was not affected by H 2S fumigation. Photosynthetic CO 2 fixation decreased linearly with time in both control and fumigated plants. The rate of decrease in CO 2 fixation was faster in the fumigated plants; after 14 days of exposure the fumigated plants showed a decrease in CO 2 fixation of 23%äs compared with the control plants. The H 2S-induced decrease in CO 2 fixation was accompanied by a decrease in quenching of the chlorophyll fluorescence. The most characteristic change in chlorophyll fluorescence was a decreased difference between maximum and steady-state fluorescence [(P-T)/P), suggesting a reduced efficiency in the use of photochemical energy in photosynthesis. Differences in CO 2 fixation were more pronounced whcn measured at high light intensity; the maximum rate of CO 2 fixation at light saturation decreased significantly with time in the H 2S-exposed plants; after 14 days of H 2S exposure a decrease of more than 70% was noted. The decrease in CO 2 fixation could not be attributed to a decreased chlorophyll content; on the contrary, chlorophyll content even slightly increased during fumigation. The initial increase in CO 2 fixation rate with increasing light intensity was also reduced by prolonged H 2S fumigation, indicating an effect of H 2S fumigation on photosynthetic electron transport. Finally, the phytotoxicity of H 2S is discusscd in relation to the H 2S-induced changes in photosynthetic CO 2 fixation and chlorophyll a fluorescence, and the effect of H 2S on leaf development observed in earlier studies. 相似文献
7.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is the clinical syndrome of persistent lung inflammation caused by various direct and indirect stimuli. Despite advances in the understanding of disease pathogenesis, few therapeutic have emerged for ALI/ARDS. Thus, in the present study we evaluated the therapeutic potential of ethyl gallate (EG), a plant flavanoid in the context of ALI using in vivo (BALB/c) and in vitro models (human monocytes). Our in vivo data supports the view that EG alleviates inflammatory condition in ALI as significant reduction in BALF neutrophils, ROS, proinflammatory cytokines and albumin levels were observed with the single i. p of EG post LPS exposure. Also, histochemical analysis of mice lung tissue demonstrated that EG restored LPS stimulated cellular influx inside the lung airspaces. Unraveling the mechanism of action, our RT-PCR and western blot analysis suggest that enhanced expression of HO-1 underlies the protective effect of EG on ROS level in mice lung tissue. Induction of HO-1 in turn appears to be mediated by Nrf2 nuclear translocation and consequent activation and ablation of Nrf2 activity through siRNA notably abrogated the EG induced protective effect in LPS induced human monocytes. Furthermore, our results indicate that EG generated moderate amounts of H 2O 2 could induce Nrf2 translocation in the in vitro systems. However, given the insignificant amount of H 2O 2 recorded in the injected material in the in vivo system, additional mechanism for EG action could not be excluded. Nevertheless our results highlight the protective role of EG in ALI and provide the novel insight into its usefulness as a therapeutic tool for the treatment of ALI. 相似文献
8.
Hydrogen sulfide (H 2S) is a signal molecule that is involved in plant growth, development and the acquisition of stress tolerance including heat tolerance, but the mechanism of H 2S-induced heat tolerance is not completely clear. In present study, the effect of sodium hydrosulfide (NaHS), a H 2S donor, treatment on heat tolerance of maize seedlings in relation to antioxidant system was investigated. The results showed that NaHS treatment improved survival percentage of maize seedlings under heat stress in a concentration-dependent manner, indicating that H 2S treatment could improve heat tolerance of maize seedlings. To further study mechanism of NaHS-induced heat tolerance, catalase (CAT), guaiacol peroxidase (GPX), superoxide dismutase (SOD), glutathione reductase (GR) and ascorbate peroxidase (APX) activities, and glutathione (GSH) and ascorbic acid (AsA) contents in maize seedlings were determined. The results showed that NaHS treatment increased the activities of CAT, GPX, SOD and GR, and GSH and AsA contents as well as the ratio of reduced antioxidants to total antioxidants [AsA/(AsA+DHA) and GSH/(GSH +GSSG)] in maize seedlings under normal culture conditions compared with the control. Under heat stress, antioxidant enzymes activities, antioxidants contents and the ratio of the reduced antioxidants to total antioxidants in control and treated seedlings all decreased, but NaHS-treated seedlings maintained higher antioxidant enzymes activities and antioxidants levels as well as the ratio of reduced antioxidants to total antioxidants. All of above-mentioned results suggested that NaHS treatment could improve heat tolerance of maize seedlings, and the acquisition of this heat tolerance may be relation to enhanced antioxidant system activity. 相似文献
9.
我们以往的研究工作证实了硫化氢(hydrogen sulfide,H2S)对甲醛神经毒性和氧化应激具有拮抗作用.Paraoxonase-1(PON-1)是机体重要的内源性抗氧化剂.本研究的目的是探讨PON-1是否可介导H2S的抗甲醛神经毒性作用.采用甲醛损伤PC12细胞为甲醛神经毒性的细胞模型.硫氢化钠(NaHS,一种H2S的供体)不仅可以上调PC12细胞PON-1的活力,还可恢复甲醛对PC12细胞PON-1表达与活力的抑制作用.2-hydroxyquinoline(2-HQ)是一种选择性PON-1抑制剂,它可显著降低H2S对甲醛细胞毒性、凋亡和活性氧(reactive oxygen species,ROS)累积的抑制作用.而且,2-HQ可阻止H2S逆转甲醛激活PC12细胞caspase-3和下调PC12细胞bcl-2表达.结果提示H2S依赖PON-1去保护PC12细胞对抗甲醛的神经毒性.我们的这一发现表明PON-1有希望成为防治甲醛神经损伤的新靶点. 相似文献
10.
A growing body of evidence suggests that hydrogen sulfide (H 2S) is a signaling molecule in mammalian cells. In the cardiovascular system, H 2S enhances vasodilation and angiogenesis. H 2S-induced vasodilation is hypothesized to occur through ATP-sensitive potassium channels (K ATP); however, we recently demonstrated that it also increases cGMP levels in tissues. Herein, we studied the involvement of cGMP-dependent protein kinase-I in H 2S-induced vasorelaxation. The effect of H 2S on vessel tone was studied in phenylephrine-contracted aortic rings with or without endothelium. cGMP levels were determined in cultured cells or isolated vessel by enzyme immunoassay. Pretreatment of aortic rings with sildenafil attenuated NaHS-induced relaxation, confirming previous findings that H 2S is a phosphodiesterase inhibitor. In addition, vascular tissue levels of cGMP in cystathionine gamma lyase knockouts were lower than those in wild-type control mice. Treatment of aortic rings with NaHS, a fast releasing H 2S donor, enhanced phosphorylation of vasodilator-stimulated phosphoprotein in a time-dependent manner, suggesting that cGMP-dependent protein kinase (PKG) is activated after exposure to H 2S. Incubation of aortic rings with a PKG-I inhibitor (DT-2) attenuated NaHS-stimulated relaxation. Interestingly, vasodilatory responses to a slowly releasing H 2S donor (GYY 4137) were unaffected by DT-2, suggesting that this donor dilates mouse aorta through PKG-independent pathways. Dilatory responses to NaHS and L-cysteine (a substrate for H 2S production) were reduced in vessels of PKG-I knockout mice (PKG-I−/−). Moreover, glibenclamide inhibited NaHS-induced vasorelaxation in vessels from wild-type animals, but not PKG-I−/−, suggesting that there is a cross-talk between K ATP and PKG. Our results confirm the role of cGMP in the vascular responses to NaHS and demonstrate that genetic deletion of PKG-I attenuates NaHS and L-cysteine-stimulated vasodilation. 相似文献
11.
Remodeling by its very nature implied synthesis and degradation of extracellular matrix (ECM) proteins. Although oxidative
stress, matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) have been implicated in vascular remodeling,
the differential role of MMPs versus TIMPs and oxidative stress in vascular remodeling was unclear. TIMP-3 induced vascular
cell apoptosis, therefore, we hypothesized that during vascular injury TIMP-3, MMP-9 and -12 (elastin-degrading MMP) were
increased, whereas MMP-2 (constitutive MMP) and TIMP-4 (cardioprotective TIMP) decreased. Because of the potent anti-oxidant,
vasorelaxing, anti-hypertensive agent, hydrogen sulfide (H 2S) was used to mitigate the vascular remodeling due to the differential expression of MMP and TIMP. Carotid artery injury
was created by inserting a PE-10 catheter and rotating several times before pulling out. The insertion hole was sealed. Mice
were grouped: wild type (WT), wild-type damaged artery (WTD), WT + NaHS (sodium hydrogen sulfide, precursor of H 2S) treatment (30 μmol/L in drinking water/6 weeks) and WTD + NaHS treatment. Carotid arteries were analyzed for oxidative
stress and remodeling, by measuring super oxide dismutase-1 (SOD1), p47 (NADPH oxidase subunit), nitrotyrosine, MMPs and TIMPs
by in situ immunolabeling and by Western blot analyses. The results suggested robust increase in p47, nitrotyrosine, MMP-9,
MMP-12, TIMP-3 and decrease in SOD1 and MMP-2 levels in the injured arteries. The treatment with H 2S ameliorated these effects. We concluded that p47, TIMP-3, MMP-9 and -12 were increased where as SOD-1, MMP-2 and TIMP-4
were decreased in the injured arteries. The treatment with H 2S mitigated the vascular remodeling by normalizing the levels of redox stress, MMPs and TIMPs. 相似文献
12.
Cystathionine gamma-lyase (CSE)-derived hydrogen sulfide (H2S) plays an essential role in preserving cardiac functions. Angiotensin-converting enzyme 2 (ACE2) acts as the negative regulator of the renin-angiotensin system, exerting anti-oxidative stress and anti-inflammatory properties within the body. The interplays of CSE/H2S signaling and ACE2 in cardiac aging are unclear. In this study, the regulatory roles of H2S on ACE2 expression in mouse heart tissue and rat cardiomyocytes under different stress conditions were investigated. It was found that ACE2 protein level was lower in heart tissues from old mice (56-week-old) than young mice (8-week-old), and the knockout of CSE (CSE KO) induced moderate oxidative stress and further inhibited ACE2 protein level in mouse hearts at both young and old age. Incubation of rat cardiac cells (H9C2) with a low dose of H2O2 (50 µM) suppressed ACE2 protein level and induced cellular senescence, which was completely reversed by co-incubation with 30 µM NaHS (a H2S donor). Prolonged nutrient excess is an increased risk of heart disorders by causing metabolic dysfunction and cardiac remodeling. We further found high-fat diet feeding stimulated ACE2 expression and induced severe oxidative stress in CSE KO heart in comparison with wild-type heart. Lipid overload in H9C2 cells to mimic a status of nutrient excess also enhanced the expression of ACE2 protein and induced severe oxidative stress and cell senescence, which were significantly attenuated by the supplementation of exogenous H2S. Furthermore, the manipulation of ACE2 expression partially abolished the protective role of H2S against cellular senescence. These results demonstrate the dynamic roles of H2S in the maintenance of ACE2 levels under different levels of oxidative stress, pointing to the potential implications in targeting the CSE/H2S system for the interruption of aging and diabetes-related heart disorders. 相似文献
13.
Broad range of selectivity possesses serious limitation for the development of matrix metalloproteinase-2 (MMP-2) inhibitors for clinical purposes. To develop potent and selective MMP-2 inhibitors, initially multiple molecular modeling techniques were adopted for robust design. Predictive and validated regression models (2D and 3D QSAR and ligand-based pharmacophore mapping studies) were utilized for estimating the potency whereas classification models (Bayesian and recursive partitioning analyses) were used for determining the selectivity of MMP-2 inhibitors over MMP-9. Bayesian model fingerprints were used to design selective lead molecule which was modified using structure-based de novo technique. A series of designed molecules were prepared and screened initially for inhibitions of MMP-2 and MMP-9, respectively, as these are designed followed by other MMPs to observe the broader selectivity. The best active MMP-2 inhibitor had IC 50 value of 24 nM whereas the best selective inhibitor (IC 50 = 51 nM) showed at least 4 times selectivity to MMP-2 against all tested MMPs. Active derivatives were non-cytotoxic against human lung carcinoma cell line—A549. At non-cytotoxic concentrations, these inhibitors reduced intracellular MMP-2 expression up to 78% and also exhibited satisfactory anti-migration and anti-invasive properties against A549 cells. Some of these active compounds may be used as adjuvant therapeutic agents in lung cancer after detailed study. 相似文献
14.
Haishengsu (HSS) is a seashell protein extracted from Tegillarca L. granosa, a type of Malaysian shellfish. Previous in vitro studies showed that HSS might possess biological anticancer activity. In
this combined in vitro and in vivo study, we investigated the inhibitory effects of HSS on tumor growth, invasion, and metastasis
using human lung carcinoma cell lines A549 and NCI-H292, both intensely positive for matrix metalloproteinases-2 (MMP-2) and
MMP-9. HSS significantly inhibited the proliferation of A549 and NCI-H292 as estimated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium
bromide assay. The transwell chamber assay showed that HSS effectively blocked the invasion and migration of the carcinoma
cells through the reconstituted extracellular matrix (Matrigel). Gelatin zymography analysis revealed that the secretion and
activity of MMP-2 and MMP-9 in the supernatants of the cultured cells A549 and NCI-H292 were decreased after treatment with
HSS. The levels of MMP-2 and MMP-9 in these cancer cells were further examined by Western blot assay in which a significant
decrease of MMP-2 and MMP-9 was observed in A549 and NCI-H292 cells after 24 h of exposure to HSS. The anticancer activity
of HSS was verified in a mouse model in which HSS delayed the growth of A549 xenografts after 3 weeks of oral administration.
Inhibition of MMP-2 and MMP-9 expression was also demonstrated in the A549 xenografts as determined by Western blot analysis.
These results suggest that HSS is a novel seashell protein that cannot only inhibit tumor growth but also prevent tumor invasion
and metastasis through suppressing the activity of MMP-2 and MMP-9. 相似文献
16.
Imbalance of macrophage polarization plays an indispensable role in acute lung injury (ALI), which is considered as a promising target. Matrix metalloproteinase-9 (MMP-9) is expressed in the macrophage, and has a pivotal role in secreting inflammatory cytokines. We reported that saquinavir (SQV), a first-generation human immunodeficiency virus-protease inhibitor, restricted exaggerated inflammatory response. However, whether MMP-9 could regulate macrophage polarization and inhibit by SQV is still unknown. We focused on the important role of macrophage polarization in CLP (cecal ligation puncture)-mediated ALI and determined the ability of SQV to maintain M2 over M1 phenotype partially through the inhibition of MMP-9. We also performed a limited clinical study to determine if MMP-9 is a biomarker of sepsis. Lipopolysaccharide (LPS) increased MMP-9 expression and recombinant MMP-9 (rMMP-9) exacerbated LPS-mediated M1 switching. Small interfering RNA to MMP-9 inhibited LPS-mediated M1 phenotype and SQV inhibition of this switching was reversed with rMMP-9, suggesting an important role for MMP-9 in mediating LPS-induced M1 phenotype. MMP-9 messenger RNA levels in peripheral blood mononuclear cells of these 14 patients correlated with their clinical assessment. There was a significant dose-dependent decrease in mortality and ALI after CLP with SQV. SQV significantly inhibited LPS-mediated M1 phenotype and increased M2 phenotype in cultured RAW 264.7 and primary murine bone marrow-derived macrophages as well as lung macrophages from CLP-treated mice. This study supports an important role for MMP-9 in macrophage phenotypic switching and suggests that SQV-mediated inhibition of MMP-9 may be involved in suppressing ALI during systemic sepsis.Subject terms: Inflammatory diseases, Inflammatory diseases 相似文献
18.
Sinomenine (SIN) is a bioactive alkaloid extracted from the Chinese medicinal plant Sinomenium acutum, which is widely used in the clinical treatment of rheumatoid arthritis (RA). However, its role in acute lung injury (ALI) is unclear. In this study, we investigate the role of SIN in lipopolysaccharide (LPS)-induced ALI in mice. After ALI, lung water content and histological signs of pulmonary injury were attenuated, whereas the PaO 2/FIO 2 (P/F) ratios were elevated significantly in the mice pretreated with SIN. Additionally, SIN markedly inhibited inflammatory cytokine TNF-α and IL-1β expression levels as well as neutrophil infiltration in the lung tissues of the mice. Microarray analysis and real-time PCR showed that SIN treatment upregulated adenosine A 2A receptor (A 2AR) expression, and the protective effect of SIN was abolished in A 2AR knockout mice. Further investigation in isolated mouse neutrophils confirmed the upregulation of A 2AR by SIN and showed that A 2AR-cAMP-PKA signaling was involved in the anti-inflammatory effect of SIN. Taken together, these findings demonstrate an A 2AR-associated anti-inflammatory effect and the protective role of SIN in ALI, which suggests a potential novel approach to treat ALI. 相似文献
19.
Sphaerophysa kotschyana is a Turkish endemic and endangered plant that grows near Salt Lake, in Konya, Turkey. However, little is known about the ability of this plant to generate/remove reactive oxygen species (ROS) or its adaptive biochemical responses to saline environments. After exposure of S. kotschyana to 0, 150, and 300 mM NaCl for 7 and 14 days, we investigated (1) the activities and isozyme compositions of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), ascorbate peroxidase (APX), and glutathione reductase (GR); (2) the oxidative stress parameters NADPH oxidase (NOX) activity, lipid peroxidation (MDA), total ascorbate (tAsA) content, and total glutathione content (tGlut); and (3) ROS levels for superoxide anion radical (O 2 ·? ), hydrogen peroxide (H 2O 2), hydroxyl radicals (OH·), and histochemical staining of O 2 ·? and H 2O 2. H 2O 2 content increased after 14 days of salt stress, which was consistent with the results from histochemical staining and NOX activity measurements. In contrast, oxidative stress induced by 150 mM NaCl was more efficiently prevented, as indicated by low malondialdehyde (MDA) levels and especially at 7 days, by increased levels of SOD, POX, APX, and GR. However, at 300 mM NaCl, decreased levels of protective enzymes such as SOD, CAT, POX, and GR, particularly with long-term stress (14 days), resulted in limited ROS scavenging activity and increased MDA levels. Moreover, at 300 mM NaCl, the high H 2O 2 content caused oxidative damage rather than inducing protective responses against H 2O 2. These results suggest that S. kotschyana is potentially tolerant to salt-induced damage only at low salt concentrations. 相似文献
20.
Exposure of bovine pulmonary artery smooth muscle plasma membrane suspension with the oxidant H 2O 2 (1 mM) stimulated Ca 2+ATPase activity. We sought to determine the role of matrix metalloprotease-2 (MMP-2) in stimulating Ca 2+ATPase activity by H 2O 2 in the smooth muscle plasma membrane. The smooth muscle membrane possesses a Ca 2+-dependent protease activity in the gelatin containing zymogram having an apparent molecular mass of 72 kDa. The 72 kDa protease
activity was found to be inhibited by EGTA, 1: 10-phenanthroline, a2-macroglobulin and tissue inhibitor of metalloprotease-2
(TIMP-2) indicating that the Ca 2+-dependent 72 kDa protease is the MMP-2. Western immunoblot studies of the membrane suspension with polyclonal antibodies
of MMP-2 and TIMP-2 revealed that MMP-2 and TIMP-2, respectively, are the ambient matrix metalloprotease and the corresponding
tissue inhibitor of metalloprotease in the membrane.
In addition to increasing the Ca 2+ATPase activity, H 2O 2 also enhanced the activity of the smooth muscle plasma membrane associated protease activity as evidenced by its ability
to degrade 14C-gelatin. The protease activity and the Ca 2+ATPase activity were prevented by the antioxidant, vitamin E, indicating that the effect produced by H 2O 2 was due to reactive oxidant species(es). Both basal and H 2O 2 stimulated MMP-2 activity and Ca 2+ATPase activity were inhibited by the general inhibitors of matrix metalloproteases: EGTA, 1: 10-phenanthroline, α 2-macroglobulin and also by TIMP-2 (the specific inhibitor of MMP-2) indicating that H 2O 2 increased MMP-2 activity and that subsequently stimulated Ca 2+ATPase activity in the plasma membrane. This was further confirmed by the following observations: (i) adding low doses of
MMP-2 or H 2O 2 to the smooth muscle membrane suspension caused submaximal increase in Ca 2+ATPase activity, and pretreatment with TIMP-2 prevents the increase in Ca 2+ATPase activity; (ii) combined treatment of the membrane with low doses of MMP-2 and H 2O 2 augments further the Ca 2+ATPase activity caused by the respective low doses of either H 2O 2 or MMP-2; and (iii) pretreatment with TIMP-2 prevents the increase in Ca 2+ATPase activity in the membrane caused by the combined treatment of MMP-2 and H 2O 2. 相似文献
|