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PubMed2002

CD154-CD40 T-cell costimulation pathway is required in the mechanism of hepatic ischemia/reperfusion injury, and its blockade facilitates and depends on heme oxygenase-1 mediated cytoprotection.

BACKGROUND: Ischemia/reperfusion (I/R) injury remains an important clinical problem that affects both early and later allograft outcome. This study was designed to analyze the role of T cells and CD154-CD40 T- cell costimulation pathway in a mouse liver I/R model. METHODS AND RESULTS: Ninety minutes of warm ischemia followed by 4 h of reperfusion in wild-type (WT) mice resulted in a significant hepatic damage, as assessed by liver function (serum alanine aminotransferase [sALT] levels), local neutrophil accumulation (myeloperoxidase activity), and histology (Suzuki's score). In contrast, T-cell deficiency (in T-cell deficient [nu/nu] mice), disruption of the CD154 signaling (in knockout [KO] mice), or its blockade in WT recipients (after MR1 monoclonal antibody [mAb] treatment), virtually prevented hepatic I/R insult. Unlike CD154-deficient T cells, adoptive transfer of WT spleen cells fully restored hepatic I/R injury in nu/nu mice. Finally, the improved hepatic function in CD154 KO recipients, WT mice treated with CD154 mAb, or nu/nu mice infused with CD154-deficient cells resulted in consistently enhanced expression of heme oxygenase-1 (HO-1), a heat-shock protein with cytoprotective functions. CONCLUSION: This study confirms the importance of T cells, and documents for the first time the role of CD154 costimulation signals in the mechanism of hepatic I/R injury. We also show that CD154 blockade-mediated cytoprotection results and depends on HO-1 overexpression. Our data provide the rationale for human trials to target CD154-CD40 costimulation in hepatic I/R injury, particularly in the transplant patient.

Adoptive Transfer↗
PubMed1997

Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair growth-stimulating effect.

Data from the literature indicate that nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, naproxen, piroxicam, or ibuprofen, induce hair loss in vivo. These NSAIDs are well-known inhibitors of both the cytoprotective isoform of prostaglandin endoperoxide synthase-1 (PGHS-1) and of the inducible form (PGHS-2). By immunohistochemical staining, we found that PGHS-1 is the main isoform present in the dermal papilla from normal human hair follicle (either anagen or catagen), whereas PGHS-2 was only faintly and exclusively expressed in anagen dermal papilla. Thus, PGHS-1 might be the primary target of the hair growth-inhibitory effects of NSAIDs. We thus speculated that activation of PGHS-1 might be a mechanism by which minoxidil (2,4-diamino-6-piperidinopyrimidine-3-oxyde) stimulates hair growth in vivo. We demonstrate here that minoxidil is a potent activator of purified PGHS-1 (AC50 = 80 microM), as assayed by oxygen consumption and PGE2 production. This activation was also evidenced by increased PGE2 production by BALB/c 3T3 fibroblasts and by human dermal papilla fibroblasts in culture. Our findings suggest that minoxidil and its derivatives may have a cytoprotective activity in vivo and that more potent second-generation hair growth-promoting drugs might be designed, based on this mechanism.

3T3 Cells↗
PubMedDate not supplied

Gastric cytoprotection by amoxycillin in the rat.

Amoxycillin in combination with anti-ulcer agents has been shown to prolong duodenal ulcer remission. While this effect can be related to the eradication of Helicobacter pylori, it is not known if amoxycillin might possess cytoprotective properties. Protection against ethanol-induced gastric mucosal damage by intragastric instillation of amoxycillin suspension (prepared from capsule form) and solution (from injection form, 100% pure amoxycillin), and by intraperitoneal injection of amoxycillin solution was studied using an ex vivo gastric chamber in the rat. Intragastric and intraperitoneal administration of amoxycillin dose-dependently protected the rat gastric mucosa from damage by absolute ethanol. This protection was lost when the rats were pretreated with indomethacin. Gastric mucosal blood flow as measured by laser Doppler flowmetry and gastric acid output were unaffected by amoxycillin. Amoxycillin imparts gastric cytoprotection, and one possible mechanism is by the release of prostaglandins.

Amoxicillin↗
PubMed1994

The differential mechanisms of mild irritants on adaptive cytoprotection.

The protective action of mild irritants has been established. However, the mechanisms as to how they antagonize the injurious action produced by the subsequent challenge with an ulcerogenic stimulus are still unclear. The present study examined the different protective mechanisms of an oral administration of the three mild irritants, 20% ethanol, 0.3 mol/L HCl or 5% NaCl against the gastric injurious actions of absolute ethanol in rats. In an attempt to clarify the pathways and mediators involved in the adaptive cytoprotection, [D-Pro2, D-Trp7,9]-substance P (substance P antagonist), Nw-nitro-L-arginine methyl ester (L-NAME), indomethacin, capsaicin, lidocaine, atropine or hexamethonium was given. The protective action of 20% ethanol but not the other two mild irritants, was antagonized by L-NAME, indomethacin and capsaicin, which are the inhibitors of nitric oxide (NO) and prostaglandins (PG) synthesis, and afferent sensory neuron blocker, respectively. Substance P antagonist, lidocaine or atropine given alone, prevented mucosal damage; however, only substance P antagonist enhanced the anti-lesion action of 20% ethanol, while atropine and lidocaine increased the protective effect of NaCl and HCl. The three mild irritants increased the residual gastric secretion. Only 20% ethanol and 5% NaCl but not 0.3% HCl significantly increased the basal adherent mucus and also attenuated the mucus depletion by absolute ethanol. It is concluded that the cytoprotective action of either ethanol or NaCl seems to be mediated through the increase of residual gastric secretion and adherent mucus. In the ethanol-treated group, these actions could act through the afferent sensory fibres, with NO and PG as the possible mediators.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1994

Dynamism of cytoprotective and antisecretory drugs in patients with unhealed gastric and duodenal ulcers.

A continuous multiclinical, randomized and prospective study has been carried out in our department to compare the efficacy of different cytoprotective (sucralfate, DE-NOL, Vitamin A) and antisecretory drugs (atropine, cimetidine, ranitidine, famotidine, pirenzepine) on ulcer healing in patients with chronic gastric ulcer (GU) and duodenal ulcer (DU). A total of 441 patients were randomized in different groups. The patients were treated with atropine (1 mg/day), cimetidine (1000 mg/day), ranitidine (300 mg/day), famotidine (80 mg/day), pirenzepine (50 mg/day), sucralfate (1000 mg/day), Vitamin A (3 x 50,000 IU/day) alone or in combination with cyproheptadinum (3 x 4 mg/day) DE-NOL (3 x 5 mL/day) and Tisacid (Al-Mg-hydroxycarbonicum; in different doses). Endoscopy (planimetric evaluation of ulcer sizes), measurements of clinical changes in patients' complaints, antacid consumption and laboratory tests (blood counts, urine, kidney and liver functions, electrolytes, pH status) were carried out at the beginning and 2, 4 and 6 weeks after treatment with different drugs. The incidence of ulcers, changes of ulcer sizes, subjective pain score and antacid consumption were noted at the abovementioned times. There were 20 or more patients in each group. The dynamism of ulcer healing rate was studied on the unhealed GU and DU. Our results showed that the ulcer size decreased significantly in all groups in GU and DU patients treated with cytoprotective and antisecretory drugs. Summed pain score (expressed as per cent of basic values) and antacid consumption decreased significantly in all groups. As well, some differences were found in the dynamism of ulcer healing at 2 weeks after the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Antacids↗
PubMed1992

Cytoprotection by iloprost against paracetamol-induced toxicity in hamster isolated hepatocytes.

1 The ability of iloprost (ZK36374) to protect hamster isolated hepatocytes from the toxic effects of paracetamol and its reactive metabolite N-acetyl-p-benzoquinoneimine (NABQI) was investigated. The cytoprotection provided by iloprost was compared with that of N-acetyl-L-cysteine. 2 Treatment of hepatocytes with either NABQI (0.4 mM) or paracetamol (2 mM) alone resulted in a considerable loss of cell viability, as assessed by trypan blue exclusion or leakage of lactate dehydrogenase, accompanied by an increase in the percentage of viable cells that were blebbed. N-acetyl-L-cysteine (1.25 mM) pretreatment diminished the loss of cell viability and the percentage of blebbed cells resulting from exposure to NABQI or paracetamol, whereas iloprost (10(-16) M to 10(-10) M) pretreatment reduced only the loss of cell viability, not the percentage of viable cells exhibiting blebbing. Pretreatment with N-acetyl-L-cysteine significantly attenuated the depletion by paracetamol of glutathione and decreased the covalent binding of [14C]-paracetamol to cellular proteins, whereas iloprost was without any such effects. 3 The effects of iloprost and N-acetyl-L-cysteine were also investigated by use of a model of paracetamol toxicity in which it is possible to study the biochemical events leading to cell injury separate from the generation of toxic metabolites. Hamster hepatocytes were incubated with paracetamol (4 mM) for 90 min at 37 degrees C during which metabolism of paracetamol occurs with minimal loss of cell viability. Following washing of cells, to remove paracetamol and its metabolites, there was a progressive loss of viability and increase in the percentage of cells exhibiting blebbing when incubated in buffer alone. Addition of either N-acetyl-L-cysteine (1.25 mM) or iloprost (10 14M to 10 -M), following washing, significantly reduced the expected loss of cell viability. Iloprost at concentrations outside this range was without effect.4. Paracetamol toxicity to isolated hepatocytes could be prevented or delayed by treatment with either N-acetyl-L-cysteine or iloprost, but whereas the former prevented or even reversed plasma membrane blebbing with a resultant reduction in the percentage of viable cells that were blebbed, the prostanoid appeared only to delay the progression from plasma membrane blebbing to loss of viability. Hence, the percentage of viable cells that were ultimately blebbed following exposure to paracetamol was not significantly reduced by addition of iloprost.5. Aspirin or ibuprofen exacerbated the loss of viability induced by prior incubation with paracetamol. Thus, there may be a role for endogenous prostaglandins in protecting hepatocytes from paracetamol toxicity.6. Iloprost is cytoprotective without any effect upon toxin metabolism or detoxication. The mechanism of action of iloprost probably does not involve induction of prostaglandin synthesis or activation of the previously-characterized prostacyclin receptor.

Acetaminophen↗
PubMed2004

Cytoprotection by darbepoetin/epoetin alfa in pig tubular and mouse mesangial cells.

BACKGROUND: Erythropoietin has recently been found to have cytoprotective effects in the central nervous system (CNS) and retina. The purpose of this study was to determine if darbepoetin alfa (DA) has cytoprotective properties in renal tissues. METHODS: DA was studied in LLC/PK1 and mesangial cells. Renal cellular injury was induced in different experiments by prostaglandin D2 synthase (PGDS), camptothecin, hydrogen peroxide, and hypoxia. Cellular proliferation and apoptosis were measured [apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick end-labeling (TUNEL) assay or by caspase-3 activity]. In a separate experiment, an inactive form of erythropoietin alfa was used to study receptor effects. RESULTS: DA protected against the antiproliferative effects of PGDS. In both LLC/PK1 (TUNEL and caspase-3) and mesangial cells (TUNEL), DA reduced the apoptotic stimulus of PGDS. Epoetin alfa was also found to reduce apoptosis. In LLC/PK1 cells, DA reduced apoptosis induced by camptothecin, but not hydrogen peroxide. DA reduced LLC/PK1 apoptosis induced by hypoxia when added 24 hours before hypoxia, but not when given concurrent with the hypoxic stimulus. Erythropoietin inactive did not protect against PGDS-induced apoptosis. CONCLUSION: DA has renal antiapoptotic effects for both toxic and hypoxic stimuli. The effect may be mediated via the Erythropoietin receptor.

Animals↗
PubMed1996

Possible cytoprotective mechanism in rats of D-002, an anti-ulcerogenic product isolated from beeswax.

D-002 is an anti-ulcerogenic product, isolated from beeswax, which consists of a well-defined mixture of higher primary aliphatic alcohols. It is highly effective against ethanol-induced ulcers. This study was designed to determine if D-002 shows cytoprotective properties on gastric mucosa in ethanol-induced ulcers. The involvement of endogenous prostaglandins in the protective effect of D-002 was also investigated. When a subulcerogenic dose of indomethacin (10 mg kg-1) was injected simultaneously with oral administration of ethanol, oral pre-treatment with D-002 (5-100 mg kg-1) partially inhibited the gastric protection. D-002 (5 and 25 mg kg-1) administered to normal rats significantly increased the soluble mucus content and also prevented its reduction in rats with ethanol-induced ulcers. In addition, D-002 administered at 5 and 25 mg kg-1 prevented the increase of vascular permeability induced by ethanol (60%) and reduced the concentration of thromboxane B2 (TXB2) in gastric mucosa of rats with ethanol-induced ulcers. These results support the hypothesis that the anti-ulcerogenic properties of D-002 could be related to a cytoprotective mechanism.

Animals↗
PubMed2004

Cytoprotective effect of sodium orthovanadate on ischemia/reperfusion-induced injury in the rat heart involves Akt activation and inhibition of fodrin breakdown and apoptosis.

In a rat model of myocardial ischemic infarction, sodium orthovanadate rescued cells from ischemia/reperfusion injuries. Rats underwent 30 min of myocardial ischemia by occluding the left coronary artery followed by 24 h of reperfusion. Post-treatment with orthovanadate reduced infarct size in a dose-dependent manner. Orthovanadate treatment also ameliorated contractile dysfunction of the left ventricle 72 h after reperfusion. The cytoprotective action of orthovanadate treatment was closely associated with inhibition of fodrin breakdown. Since orthovanadate is a potent inhibitor for protein tyrosine phosphatases, thereby activating tyrosine kinases and phosphatidylinositol 3-kinase (PI3K) pathways, we investigated activities of protein kinase B (Akt), a downstream target of PI3K in cardiomyocytes. Orthovanadate-induced cytoprotection was associated with partial restoration of reduced Akt activity following myocardial infarction. Restoration of Akt activity by orthovanadate treatment correlated positively with increased phosphorylation of glycogen synthase kinase-3beta and Bad in cardiomyocytes. Furthermore, orthovanadate treatment inhibited caspase-3 activation induced by ischemia. Taken together, orthovanadate post-treatment rescued cardiomyocytes from ischemia/reperfusion injuries via Akt activation and inhibition of fodrin breakdown, thereby inhibiting apoptosis.

Animals↗
PubMed2004

Cytoprotective efficacy and mechanisms of the liposoluble iron chelator 2,2'-dipyridyl in the rat photothrombotic ischemic stroke model.

We examined the efficacy of the liposoluble iron chelator 2,2'-dipyridyl (DP) in reducing histological damage in rats submitted to cerebral ischemia and the mechanisms involved in the potential cytoprotection. For this purpose, DP (20 mg/kg, i.p.) was administered 15 min before and 1 h after induction of cortical photothrombotic vascular occlusion in rat. Histological studies were performed to assess infarct volume (at days 1 and 3 postischemia) and astromicroglial activation (at day 3 postischemia). Damage to endothelial and neuronal cells was evaluated at day 1 postischemia by quantitative measurements of Evans Blue extravasation and N-acetylaspartate levels, respectively. Cerebral blood flow was recorded in the ischemic core by laser-Doppler flowmetry within the 15 min to 2 h period after photothrombosis. At 4-h postischemia, radical oxygen species (ROS) production was evaluated by measuring brain glutathione concentrations. The cortical expression of the proteins heme oxygenase-1 (HO-1) and hypoxia-inducible factor-1alpha (HIF-1alpha) was analyzed by Western blotting at day 1 postischemia. Infarct volume and ischemic damage to endothelial and neuronal cells were significantly reduced by DP treatment. This cytoprotection was associated with a reduction in ROS production, perfusion deficits, and astrocytic activation. DP treatment also resulted in significant changes in HO-1 (+100%) and HIF-1alpha (-50%) protein expression at the level of the ischemic core. These results report the efficacy of the liposoluble iron chelator DP in reducing histological damage induced by permanent focal ischemia.

2,2'-Dipyridyl↗
PubMed1981

Sulfhydryl compounds may mediate gastric cytoprotection.

Ethanol induces hemorrhagic gastric erosions and causes a dose-dependent decrease in the concentration of nonprotein sulfhydryl compounds in rat gastric mucosa. Sulfhydryl-containing drugs protect rats from ethanol-induced gastric erosions, whereas sulfhydryl blocking agents counteract the mucosal cytoprotective effect of prostaglandin F2 beta. These observations suggest that endogenous nonprotein sulfhydryls may mediate prostaglandin-induced gastric cytoprotection and that sulfhydryl drugs may have potential for preventing or treating hemorrhagic gastric erosions.

Animals↗
PubMed1981

Role of mucosal prostaglandins and DNA synthesis in gastric cytoprotection by luminal epidermal growth factor.

This study compares the effect of epidermal growth factor and prostaglandins (PGE2 or PGI2), applied topically to gastric mucosa, on gastric secretion and formation of ASA-induced gastric ulcerations in rats. Epidermal growth factor given topically in non-antisecretory doses prevented dose-dependently the formation of ASA-induced ulcers without affecting prostaglandin generation but with a significant rise in DNA synthesis in the oxyntic mucosa. The anti-ulcer effect of topical prostaglandins was also accompanied by an increase in DNA synthesis. This study indicates that topical epidermal growth factor, like PGE2 or PGI2, is cytoprotective and that this cytoprotection is not mediated by the inhibition of gastric secretion or prostaglandin formation but related to the increase in DNA synthesis in oxyntic mucosa.

Animals↗
PubMed2002

Cytoprotection by propolis ethanol extract of acute absolute ethanol-induced gastric mucosal lesions.

Acute p.o. administration of absolute ethanol (1.0 ml/kg) to fasted rats produced extensive necrosis of gastric mucosa. Pretreatment with p.o. administration of propolis ethanol extract (PEE) could effectively and dose-dependently prevent such necrosis. This protective effect is called "cytoprotection. "The maximal cytoprotective effect against absolute ethanol (AE)-induced gastric mucosal lesion was observed 1 hour after PEE administration. A gross examination of the gastric mucosa showed a marked improvement in groups receiving PEE. In order to further investigate the gastric protective mechanism of PEE, lipid peroxidation (LPO) levels in vivo and in vitro were estimated. PEE exhibited dose-dependent superoxide scavenging activity and antioxidant effects on AE-induced LPO in rat gastric mucosal homogenates. It was concluded that the gastric protective mechanism of PEE was due, at least in part, to its ability to inhibit LPO, and hence indirectly protect the gastric mucosa from oxidative stress.

Administration, Oral↗
PubMed2003

Role of PGE2 on gallbladder muscle cytoprotection of guinea pigs.

H2O2 and taurochenodeoxycholic acid (TCDC) impair the contraction induced by CCK-8, ACh, and KCl without affecting the actions of PGE2 and damage functions of membrane proteins except for PGE2 receptors. The aim of this study was to examine whether the preserved PGE2 actions contribute to cytoprotective mechanisms against reactive oxygen species. Muscle cells from guinea pig gallbladder were obtained by enzymatic digestion. Levels of lipid peroxidation and activities of SOD and catalase were determined by spectrophotometry. Pretreatment with PGE2 prevented the inhibition of H2O2 or TCDC on agonist (CCK-8, ACh, and KCl)-induced contraction and reduced the expected increase in lipid peroxidation and activities of catalase and SOD caused by H2O2 and TCDC. Incubation with CCK-8 for 60 min desensitized CCK-1 receptors up to 30 min, whereas no receptor desensitization was observed after PGE2 pretreatment. Cholesterol-rich liposome treatment enhanced the inhibition of H2O2 and TCDC on agonists-induced contraction, including that of PGE2. Pretreatment with PGE2 before H2O2 and TCDC did not completely block their inhibition on agonist-induced contraction. Cholesterol-rich liposome treatment impaired the expected increase in catalase activities in response to PGE2. We conclude that pretreatment with PGE2 prevents the muscle cell damage caused by H2O2 and TCDC due to the resistance of PGE2 receptors to agonist-induced desensitization. The preservation of PGE2 receptors may be designed to conserve these cytoprotective functions that are, however, impaired by the presence of excess cholesterol in the plasma membrane.

Acetylcholine↗
PubMed2000

Simple epithelial keratins are dispensable for cytoprotection in two pancreatitis models.

Pancreatic acinar cells express keratins 8 and 18 (K8/18), which form cytoplasmic filament (CF) and apicolateral filament (ALF) pools. Hepatocyte K8/18 CF provide important protection from environmental stresses, but disruption of acinar cell CF has no significant impact. We asked whether acinar cell ALF are important in providing cytoprotective roles by studying keratin filaments in pancreata of K8- and K18-null mice. K8-null pancreas lacks both keratin pools, but K18-null pancreas lacks only CF. Mouse but not human acinar cells also express apicolateral keratin 19 (K19), which explains the presence of apicolateral keratins in K18-null pancreas. K8- and K18-null pancreata are histologically normal, and their acini respond similarly to stimulated secretion, although K8-null acini viability is reduced. Absence of total filaments (K8-null) or CF (K18-null) does not increase susceptibility to pancreatitis induced by caerulein or a choline-deficient diet. In normal and K18-null acini, K19 is upregulated after caerulein injury and, unexpectedly, forms CF. As in hepatocytes, acinar injury is also associated with keratin hyperphosphorylation. Hence, K19 forms ALF in mouse acinar cells and helps define two distinct ALF and CF pools. On injury, K19 forms CF that revert to ALF after healing. Acinar keratins appear to be dispensable for cytoprotection, in contrast to hepatocyte keratins, despite similar hyperphosphorylation patterns after injury.

Actins↗
PubMed1996

5-HT in DVC: disparate effects on TRH analogue-stimulated gastric acid secretion, motility, and cytoprotection.

Convergent evidence suggests that thyrotropin-releasing hormone (TRH) is a principal regulator of several vagally mediated gastric responses. Serotonin (5-HT) interacts with TRH in the dorsal vagal complex (DVC) to augment gastric acid secretory responses. This study investigated the ability of 5-HT to alter other gastric responses mediated by TRH administration into the DVC. Co-injection of 5-HT (7.9 pmol) and the TRH analogue RX-77368 (0.66 pmol) produced a 117% enhancement in 1-h gastric acid output compared with rats treated with RX-77368 (0.66 pmol) alone into the DVC. In contrast, coadministration of RX-77368 (4 pmol) with various doses of 5-HT (0.0048-480 pmol) was ineffective in significantly altering stimulation of gastric antral motility produced by RX-77368 (4 pmol) alone. The effect of a lower dose of DVC RX-77368 (0.66 pmol) on gastric motility was also not changed by 5-HT coadministration. Moreover, the cytoprotective effect of DVC RX-77368 (1.5 pmol) on oral ethanol-induced gastric mucosal lesions was reversed by 5-HT coadministration (54 or 18 pmol). The results suggest that activation of 5-HT receptors in the DVC can augment, not affect, and attenuate DVC TRH analogue-stimulated gastric acid secretion, antral motility, and cytoprotection, respectively.

Animals↗
PubMed1991

Transient ischemia or heat stress induces a cytoprotectant protein in rat kidney.

Sublethal heat exposure induces the production of heat stress protein (HSP) 72 kDa, a reported cytoprotectant, in several tissues including the rat kidney. However, the localization and time course of HSP 72 accumulation in the kidney in response to heat or other cell stresses such as transient ischemia have not been described. In anesthetized rats exposed to either 42 +/- 0.5 degrees C (heat stress) or 37 degrees C (sham) for 15 min, accumulation of HSP 72 in kidney homogenates, detected by immunoblot analysis using a specific monoclonal anti-HSP 72 antibody, peaked 4-6 h after heat stress and persisted for 10 days. HSP 72 appeared rapidly in renal papilla within 1 h and in medulla and cortex within 4 h after heat stress. No HSP 72 was detected in tissues from sham heat stress. HSP 72 was also detected within 3 h of at least 15 min of renal ischemia in situ. Accumulation was maximal after 60 min of ischemia and persisted for 5 days, whereas no HSP 72 was detected after 90 min of ischemia or in the contralateral nonischemic kidney at any time point. This study demonstrates that transient ischemia, like heat stress, results in the rapid cytosolic accumulation of HSP 72, a known cytoprotectant that may be important in mediating cell repair or increasing resistance to subsequent injury.

Animals↗