Escin attenuates cerebral edema induced by acute omethoate poisoning

Organophosphorus exposure affects different organs such as skeletal muscles, the gastrointestinal tract, liver, lung, and brain. The present experiment aimed to evaluate the effect of escin on cerebral edema induced by acute omethoate poisoning. Sprague-Dawley rats were administered subcutaneously with omethoate at a single dose of 60 mg/kg followed by escin treatment. The results showed that escin reduced the brain water content and the amount of Evans blue in omethoate-poisoned animals. Treatment with escin decreased the levels of tumor necrosis factor-alpha (TNF-α), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and prostaglandin E? (PGE?) in the brain. Escin also alleviated the histopathological change induced by acute omethoate poisoning. The findings demonstrated that escin can attenuate cerebral edema induced by acute omethoate poisoning, and the underlying mechanism was associated with ameliorating the permeability of the blood-brain barrier.     

Protective effects of Danshensu on liver injury induced by omethoate in rats

This study was to evaluate the protective effects of Danshensu on liver injury induced by omethoate in Sprague Dawley rats. The acute omethoate poisoning model was established by administrating subcutaneously with omethoate at a single dose of 60?mg/kg. Danshensu treatment markedly inhibited the increases of aspartate aminotransferase, alanine aminotransferase, cyclooxygenase-2, tumor necrosis factor-alpha, thromboxane B₂, and thromboxane B₂/6-keto-PGF1alpha ratio induced by omethoate. The histopathological examination further confirmed that administration with Denshensu ameliorated liver injury. The results demonstrated that Danshensu possesses protective action on hepatic injury induced by omethoate and the pharmacological mechanism was related to the anti-inflammatory effect and circulation improvement of Danshensu, at least in part.     

Protective effect of reduced glutathione on the liver injury induced by acute omethoate poisoning

Omethoate is an organophosphate insecticide with high toxicity. The aim of this study was to investigate the protective effect of exogenous reduced glutathione (GSH) on omethoate-induced liver injury. Sprague-Dawley rats were randomly divided into three groups: control, OM (omethoate poisoning), and OM+GSH (omethoate poisoning treated with GSH). The activities of acetylcholinesterase (AChE), aspartate aminotransferase (AST), alanine aminotransferase (ALT) in plasma, free organophosphate (FOP) in the liver were determined, and the histopathological changes in the liver were observed. Furthermore, TNF-α and NO in liver homogenate were assayed. The results showed that AChE activity was significantly inhibited by omethoate, but was not altered by GSH treatment. GSH was able to prevent hepatocellular edema and fatty degeneration, decrease liver FOP, attenuate the increased AST and ALT activity, and decline the increase of TNF-α and NO induced by omethoate. These results indicate GSH can attenuate liver injury, and suggest that GSH may be administered to protect the organ from injury in patients with acute organophosphate poisoning.     

Effects of 4-dimethylaminophenol,Co2EDTA,or NaNO2 on cerebral blood flow and sinus blood homeostasis of dogs in connection with acute cyanide poisoning

The effects of the cyanide antidotes DMAP, Co₂EDTA, and NaNO₂ on cerebral blood flow (CBF) and cerebral blood gases were investigated in connection with acute poisoning of dogs by cyanide. The substances were injected intravenously. Local CBF as measured with thermocouples in the cingulum increased by 100–200% after a non-lethal dose of KCN (1 mg/kg) and by 50% after injection of NaNO₂ (15 mg/kg), that oxidized some 20% of the total hemoglobin to ferrihemoglobin. Co₂EDTA (10 mg/kg) induced a decrease in local CBF of 30% and in brain temperature of 0.5°C. The temperature diminished also after poisoning by KCN, but it rose by 0.15°C after the administration of NaNO₂. Local CBF and sinus sagittalis blood flow increased by 60–160% for about 15 min, and the brain temperature decreased by 0.4–0.5°C when DMAP (3.25 mg/kg) or Co₂EDTA (15 mg/kg) was injected 1 min after poisoning by cyanide (4 mg/kg), a dose that always caused respiratory arrest. Immediately after injection of DMAP the brain temperature rose transiently by 0.1–0.2°C. Co₂EDTA did not exert such an effect. In the sinus sagittalis blood of artificially ventilated animals pCO₂ decreased rapidly by 10–20 mmHg after poisoning and approached the initial level after treatment with DMAP or Co₂EDTA. The highest value of pO₂ was about 80 mmHg and 50 mmHg after injection of DMAP and Co₂EDTA, respectively; thereafter pO₂ declined to 20 mmHg or 40 mmHg at 20 min. The lactate concentration increased by 60–70% without tendency to return to normal.     

Enzyme studies with human and hen autopsy tissue suggest omethoate does not cause delayed neuropathy in man

Levels of acetylcholinesterase and neurotoxic esterase were measured in brain autopsy material. In tissue from a fatal human poisoning and from hens given 4–8 × unprotected LD₅₀ AChE was highly inhibited and neurotoxic esterase uninhibited. The findings correlate with the inhibitory power of omethoate against these enzymes in vitro. It is concluded that omethoate has negligible potential to cause delayed neuropathy and a published report of human neuropathy due to omethoate is criticised.     

脑水肿分子机制的研究进展

脑水肿是指脑内水分增加导致脑容积增大的一种病理现象,是脑组织对各种致病因素的反应。颅内损伤、缺血、缺氧、炎症、脑代谢障碍、肿瘤以及中毒都会引起脑水肿。脑水肿可导致颅内压的升高,当颅内压升高到一定程度时,脑组织就会发生功能和结构的损害,严重者导致脑死亡。先前对脑水肿发病机制的研究包括血脑屏障学说、钙离子学说、脑微循环障碍学说、脑细胞代谢障碍等。但是近年的研究表明脑水肿的发生与水通道蛋白4、基质金属蛋白酶、紧密连接蛋白、炎性细胞因子等密切相关。本文就脑水肿发生的分子机制进行综述。     

Cerebral edema induced in mice by a convulsive dose of soman. Evaluation through diffusion-weighted magnetic resonance imaging and histology

Purpose

In the present study, diffusion-weighted magnetic resonance imaging (DW-MRI) and histology were used to assess cerebral edema and lesions in mice intoxicated by a convulsive dose of soman, an organophosphate compound acting as an irreversible cholinesterase inhibitor.

Methods

Three hours and 24 h after the intoxication with soman (172 μg/kg), the mice were anesthetized with an isoflurane/N₂O mixture and their brain examined with DW-MRI. After the imaging sessions, the mice were sacrificed for histological analysis of their brain.

Results

A decrease in the apparent diffusion coefficient (ADC) was detected as soon as 3 h after the intoxication and was found strongly enhanced at 24 h. A correlation was obtained between the ADC change and the severity of the overall brain damage (edema and cellular degeneration): the more severe the damage, the stronger the ADC drop. Anesthesia was shown to interrupt soman-induced seizures and to attenuate edema and cell change in certain sensitive brain areas. Finally, brain water content was assessed using the traditional dry/wet weight method. A significant increase of brain water was observed following the intoxication.

Conclusions

The ADC decrease observed in the present study suggests that brain edema in soman poisoning is mainly intracellular and cytotoxic. Since entry of water into the brain was also evidenced, this type of edema is certainly mixed with others (vasogenic, hydrostatic, osmotic). The present study confirms the potential of DW-MRI as a non-invasive tool for monitoring the acute neuropathological consequences (edema and neurodegeneration) of soman-induced seizures.     

七叶皂苷钠对肺部急性炎性渗出的影响

目的：研究七叶皂苷钠对肺部急性炎性渗出的作用。方法：以乙酸所致的腹腔毛细血管通透性增高模型小鼠观察七叶皂苷钠对急性渗出作用的时效关系;以肾上腺素致大鼠急性肺水肿和内毒素致小鼠急性肺损伤模型,观察七叶皂苷钠对急性肺部炎症渗出的影响。结果：七叶皂苷钠抑制急性炎症渗出作用的起效较慢,给药5h后作用开始较为明显,作用可持续24h;预防给药,可明显降低急性肺水肿大鼠的死亡率;对肾上腺素及内毒素所致肺部炎症也有明显抑制作用。结论：七叶皂苷钠可用于急性肺炎中肺部急性炎症渗出的防治。     

Effects of escin on acute inflammation and the immune system in mice

Escin has been used extensively to treat chronic venous insufficiency, hemorrhoids, and edema resulting from cerebral ischemic damage, trauma or operation. However, no studies have looked at the anti-inflammatory properties of escin administered by intravenous injection, and it is still not clear whether escin has an effect on the immune system. This study seeks to investigate the time dependent anti-inflammatory properties of escin and its effect on the immune system. The anti-inflammatory effect of escin was observed in carrageenan-induced paw edema and acetic acid-induced capillary permeability in mice. The immunopharmacological effects of escin were evaluated by spleen index (SI), thymus index (TI), proliferative capacity of splenocytes (PS), lymphocyte count (LC), serum TNF-α levels, and phagocytic rate (PR) in mice. Escin treatment showed a significant anti-inflammatory effect, similar to that seen with dexamethasone treatment. However, the duration of the anti-inflammatory response was longer with escin treatment than with dexamethasone treatment. The results also demonstrated that escin had no significant effects on SI, TI, LC, PS, TNF-α levels, and PR. The findings suggest that escin is a potent anti-inflammatory drug with long-lasting anti-inflammatory effects and without any immunosuppressive effects.     

依达拉奉联合七叶皂苷钠治疗急性脑出血的临床观察

目的：探讨依达拉奉联合七叶皂苷钠治疗急性脑出血的临床研究。方法将60例急性脑出血患者按数字表法随机分为对照组和观察组,每组各30例。对照组采用常规的内科治疗,观察组在对照组基础上分别给予依达拉奉和七叶皂苷钠静脉滴注。于治疗后14 d、28 d进行神经功能恢复情况,病灶体积,临床疗效评定。结果与对照组相比治疗后14 d、28 d,观察组NIHSS评分明显低于对照组义（ t＝2．136, t＝4.117,P＜0．05,P＜0．01）。治疗后14 d,血肿、水肿差异均无统计学意义（t＝1．395,t＝0．737,均P＞0．05）;治疗后28 d,血肿、水肿差异均有统计学意义（t＝3．140,t＝2．367,P＜0．01,P＜0．05）。两组总有效率差异有统计学意义（χ2＝6．650,P＜0．01）。结论依达拉奉联合七叶皂苷钠治疗脑出血可显著改善患者的神经功能缺损、血肿吸收、临床疗效,安全可靠。     

Curcumin attenuates brain edema in mice with intracerebral hemorrhage through inhibition of AQP4 and AQP9 expression

Aim:

Aquaporins (AQPs) are the water-channels that play important roles in brain water homeostasis and in cerebral edema induced by brain injury. In this study we investigated the relationship between AQPs and a neuroprotective agent curcumin that was effective in the treatment of brain edema in mice with intracerebral hemorrhage (ICH).

Methods:

ICH was induced in mice by autologous blood infusion. The mice immediately received curcumin (75, 150, 300 mg/kg, ip). The Rotarod test scores, brain water content and brain expression of AQPs were measured post ICH. Cultured primary mouse astrocytes were used for in vitro experiments. The expression of AQP1, AQP4 and AQP9 and NF-κB p65 were detected using Western blotting or immunochemistry staining.

Results:

Curcumin administration dose-dependently reduced the cerebral edema at d 3 post ICH, and significantly attenuated the neurological deficits at d 5 post ICH. Furthermore, curcumin dose-dependently decreased the gene and protein expression of AQP4 and AQP9, but not AQP1 post ICH. Treatment of the cultured astrocytes with Fe²⁺ (10–100 μmol/L) dose-dependently increased the expression and nuclear translocation of NF-κB p65 and the expression of AQP4 and AQP9, which were partly blocked by co-treatment with curcumin (20 μmol/L) or the NF-κB inhibitor PDTC (10 μmol/L).

Conclusion:

Curcumin effectively attenuates brain edema in mice with ICH through inhibition of the NF-κB pathway and subsequently the expression of AQP4 and AQP9. Curcumin may serve as a potential therapeutic agent for ICH.     

Inhibition of central angiotensin-converting enzyme with enalapril protects the brain from ischemia/reperfusion injury in normotensive rat

Background and the Purpose of the study

Central Angiotensin Converting Enzyme (ACE) has an important role on cerebral microcirculation and metabolism. However, its role in terms of protecting the brain from ischemic/reperfusion (I/R) injury are debatable. This study evaluated the role of ACE, using enalapril as ACE inhibitor, in protection of the brain from I/R injury during transient focal cerebral ischemia (TFCI) in normotensive rat.

Method

Male Sprague Dawley rats (280–320g) randomly assigned to control ischemic and enalapril pre-treated ischemic groups. Enalapril was injected intraperitoneally 1 h before middle cerebral artery occlusion (MCAO) at the dose of 0.03 or 0.1 mg/kg. Cerebral ischemia was induced by 60 min MCAO followed by 24 hrs reperfusion. After evaluation of neurological deficit scores (NDS) the animal was sacrificed for assessment of cerebral infarction and edema.

Results

TFCI induced cerebral infarctions (283±18 mm³), brain edema (4.1±0.4%) and swelling (9.8±1.5%) with NDS of 3.11±0.36. Non-hypotensive dose of enalapril (0.03 mg/kg) improved NDS (1.37±0.26), reduced cerebral infarction (45%), brain edema (54%) and swelling of the lesioned hemispheres (34%) significantly. However, hypotensive dose of enalapril (0.1 mg/kg) could improve neurological activity (1.67±0.31) and failed to reduce cerebral infarction (276±39 mm³) and swelling (10.4±1.4%).

Conclusion

In the rat model of transient focal cerebral ischemia, inhibition of angiotensin converting enzyme with non-hypotensive doses of enalapril has the benefit of improving neurological activity, reducing cerebral infarction, brain swelling and edema of acute ischemic stroke. Therefore, it is reasonable to conclude that central renin-angiotensin system may participate in ischemic/reperfusion injury of the cerebral cortex.     

Blood brain barrier permeability and therapeutic time window of Ginkgolide B in ischemia–reperfusion injury

The goal of this study was to estimate the blood brain barrier (BBB) permeability of Ginkgolide B in normal condition and models of ischemia both in vivo and in vitro. A sensitive LC-MS/MS analytical method was developed to determinate accurately the concentration of Ginkgolide B in cell, plasma and brain tissue. The injured rat brain microvessel endothelial cells (RBMECs) induced by Na₂S₂O₄ served as a hypoxia/reoxygenation model in vitro. Intracellular concentration of Ginkgolide B increased in injured cells in a concentration-dependent manner. As a model of in vivo—ischemia/reperfusion, we performed middle cerebral artery occlusion (MCAO) in rats. Concentration of Ginkgolide B in the brain tissues showed higher in cerebral ischemia-reperfused animals than that in normal rats. To evaluate potential clinical effect of Ginkgolide B, we determined therapeutic time window in MCAO rats. Up to i.v. administration at 2 h after reperfusion of rats, Ginkgolide B could decrease infarction volume and brain edema, exerting significant protective effect in cerebral ischemia injury. In conclusion, Ginkgolide B could pass through BBB, especially after ischemia–reperfusion injury of brain, and might be therapeutically effective for ischemia/reperfusion injury of human brain.     

Multiple actions of the coumarine derivative cloricromene and its protective effects on ischemic brain injury

The effects of different doses (0.25, 0.5, 1 and 2 mg/kg/i.p.) of cloricromene, a coumarine derivative, have been investigated on brain malondialdehyde levels, brain edema, myeloperoxidase activity, survival, locomotor hyperactivity and hippocampal neuronal loss following transient cerebral ischemia induced by temporary bilateral carotid occlusion in the Mongolian gerbil. Cloricromene reduced brain lipid peroxidation, measured through the evaluation of malondialdehyde (–82.9% with the highest dose), and the formation of postischemic brain edema, evaluated by water content. The increase in myeloperoxidase activity observed in the hippocampus of postischemic animals was also reduced: 0.7±0.3 U × 10^–3 vs. 3.3±0.3 U × 10^–3/g tissue. The same treatment increased survival and reduced hyperactivity linked to neurodegeneration induced by cerebral ischemia and reperfusion. Histological observations of the pyramidal layer of CAI showed a reduction of neuronal loss in animals that received the drug before occlusion but not in those that were treated after the occlusion. These results show that cloricromene, a drug with multiple actions, improves brain injury induced by transient cerebral ischemia.     

γ-氨基丁酸对急性不完全性全脑缺血大鼠脑组织氨基酸和钙离子含量的影响(英文)

目的　进一步探讨γ 氨基丁酸 (GABA)类药物对脑缺血保护作用的机制。方法　结扎双侧颈总动脉制备大鼠不完全性全脑缺血模型 ,高效液相法和原子吸收分光光度法分别测定脑组织氨基酸和钙离子含量。结果　脑缺血 4h显著增加大鼠海马和皮层区的谷氨酸 (Glu)和天冬氨酸 (Asp)含量及海马GABA含量 ,增高皮层细胞钙离子水平和含水量。脑缺血前 30min给予GABA 10 0mg·kg- 1,iv ,能逆转缺血诱导的Glu和Asp等兴奋性氨基酸释放增加 ,减轻脑组织含水量。此外尚能增加内源性GABA含量。结论　外源性给予GABA可逆转脑缺血诱导的兴奋性氨基酸释放 ,升高抑制性氨基酸水平 ,减轻脑水肿     

Neuroprotective activity of Wedelia calendulacea on cerebral ischemia/reperfusion induced oxidative stress in rats

Objective:

This study was undertaken to evaluate the neuroprotective activity of Wedelia calendulacea against cerebral ischemia/reperfusion induced oxidative stress in the rats.

Materials and Methods:

The global cerebral ischemia was induced in male albino Wistar rats by occluding the bilateral carotid arteries for 30 min followed by 1 h and 4 h reperfusion. At various times of reperfusion, the histopathological changes and the levels of malondialdehyde (MDA), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione–s–transferase (GST), and hydrogen peroxide (H₂O₂) activity and brain water content were measured.

Results:

The ischemic changes were preceded by increase in concentration of MDA, hydrogen peroxide and followed by decreased GPx, GR, and GST activity. Treatment with W. calendulacea significantly attenuated ischemia–induced oxidative stress. W. calendulacea administration markedly reversed and restored to near normal level in the groups pre-treated with methanolic extract (250 and 500 mg/kg, given orally in single and double dose/day for 10 days) in dose-dependent way. Similarly, W. calendulacea reversed the brain water content in the ischemia reperfusion animals. The neurodegenaration also conformed by the histopathological changes in the cerebral-ischemic animals.

Conclusion:

The findings from the present investigation reveal that W. calendulacea protects neurons from global cerebral–ischemic injury in rat by attenuating oxidative stress.KEY WORDS: Brain edema, global cerebral ischemia, histopathology, oxidative stress, Wedelia calendulacea     

A novel Na+ and Ca2+ channel blocker, T-477, prevents brain edema following microsphere-induced permanent occlusion of cerebral arterioles in rats

One of the most common acute complications of stroke is brain edema. Treatment of edema is recommended when the condition of the patients is deteriorating. The present study was undertaken to evaluate the effect of T-477 [(R)-(+)-2-(4-chlorophenyl)-2,3-dihydro-4-diethyl aminoacetyl-4H-1,4-benzorthiazine hydrochloride], a novel neuronal Na+ and Ca2+ channel blocker, on brain edema in rats. Cerebral ischemia was induced by intra-arterial infusion of 1000 microspheres into the forebrain of freely moving rats, resulting in brain edema. T-477 was intravenously infused continuously for 24 h or twice for 3 h with a 3-h interval between infusions immediately after microsphere injection. T-477 dose-dependently inhibited the increase in brain water content by both infusion procedures; the inhibition was statistically significant at doses of 25 mg/kg per 24 h and 14 mg/kg per 9 h. Additionally, infusion of T-477 at a dose of 14 mg/kg per 9 h significantly inhibited the decrease in K content and the increase in Ca content of the forebrain. In conclusion, T-477 prevents brain edema following microsphere-induced cerebral embolism in rats.     

脑血疏口服液联合神经节苷脂治疗急性脑出血的疗效观察

目的观察脑血疏口服液联合神经节苷脂治疗急性脑出血的临床疗效。方法选取2012年1月—2015年12月在连云港市赣榆区人民医院接受急性脑出血治疗的患者82例,随机分成对照组和治疗组,每组各41例。对照组患者根据出血情况静脉滴注单唾液酸四己糖神经节苷脂钠注射液,50~80 m L加入到250 m L生理盐水中,1次/d,两周之后根据患者情况减量,维持20~40 m L/d。治疗组患者在对照组的基础上口服脑血疏口服液,10 m L/次,3次/d。两组患者均连续治疗1个月。比较两组患者临床疗效、脑血肿和脑水肿量减少量、神经功能缺损程度(NIHSS)评分、改良Barthel指数(BI)评分以及日常生活能力(ADL)评分变化。结果治疗后,对照组和治疗组总有效率分别为78.05%和92.68%,两组总有效率比较差异具有统计学意义(P0.05)。治疗后,两组患者脑血肿和脑水肿减少量均比治疗前明显减少(P0.05);且治疗后治疗组脑血肿和脑水肿减少量比对照组的更明显(P0.05)。治疗后,两组患者NIHSS评分比治疗前明显降低,BI和ADL评分比治疗前明显升高,同组治疗前后比较差异具有统计学意义(P0.05);且治疗组患者上述指标评分改善程度优于对照组,两组比较差异具有统计学意义(P0.05)。结论脑血疏口服液联合神经节苷脂治疗急性脑出血能有效减少患者脑血肿和脑水肿量,降低神经功能缺损程度,提高改良BI,增强日常生活能力,具有一定的临床推广应用价值。     

Ethyl pyruvate protects rats from phosgene‐induced pulmonary edema by inhibiting cyclooxygenase2 and inducible nitric oxide synthase expression

Phosgene is a poorly water‐soluble gas penetrating the lower respiratory tract which can induce acute lung injury characterized by a latent phase of fatal pulmonary edema. Pulmonary edema caused by phosgene is believed to be a consequence of oxidative stress and inflammatory responses. Ethyl pyruvate (EP) has been demonstrated to have anti‐inflammatory and anti‐oxidative properties in vivo and in vitro. The potential therapeutic role of EP in phosgene‐induced pulmonary edema has not been addressed so far. In the present study, we aim to investigate the protective effects of EP on phosgene‐induced pulmonary edema and the underlying mechanisms. Rats were administered with EP (40 mg kg^?1) and RAW264.7 cells were also incubated with it (0, 2, 5 or 10 µm ) immediately after phosgene (400 ppm, 1 min) or air exposure. Wet‐to‐dry lung weight ratio (W:D ratio), nitric oxide (NO) and prostaglandin E₂ (PGE₂) production, cyclooxygenase2 (COX‐2) and inducible nitric oxide synthase (iNOS) expression, and mitogen‐activated protein kinases activities (MAPKs) were measured. Our results showed that EP treatment attenuated phosgene‐induced pulmonary edema and decreased the level of NO and PGE₂ dose‐dependently. Furthermore, EP significantly reduced COX‐2 expression, iNOS expression and MAPK activation induced by phosgene. Moreover, specific inhibitors of MAPKs reduced COX‐2 and iNOS expression induced by phosgene. These findings suggested that EP has a protective role against phosgene‐induced pulmonary edema, which is mediated in part by inhibiting MAPK activation and subsequently down‐regulating COX‐2 and iNOS expression as well as decreasing the production of NO and PGE₂. Copyright © 2011 John Wiley & Sons, Ltd.     

丁基苯酞对大脑中动脉阻断后皮层组织中花生四烯酸释放及磷脂酶A2基因表达的影响

目的　研究丁基苯酞（dl-NBP), d-NBP和 l-NBP对大脑中动脉阻断(MCAO) 6 h后缺血区皮层中花生四烯酸(AA)释放及磷脂酶A₂（PLA₂）基因表达的影响。方法　阻断大脑中动脉起始部造成局灶性脑缺血模型。HPLC检测AA。Northern blot检测皮层中PLA₂基因表达。结果　MCAO后6 h,皮层中AA释放明显增加。于脑缺血后5 min 和120 min,给dl-NBP(10或20 mg.kg^-1) 和尼莫地平(0.5 mg.kg^-1) 可显著抑制AA的释放。d-NBP和l-NBP作用比较,显示d-NBP有与dl-NBP相似的作用,而l-NBP则无明显影响。Northern印迹结果表明,脑缺血6 h,皮层中PLA₂的基因表达增强。 dl-NBP和d-NBP(10, 20 mg.kg^-1,ip)皆可使表达降低,而l-NBP对缺血脑组织中PLA₂的基因表达的升高无明显影响。结论　dl-NBP和d-NBP可抑制MCAO后脑组织中AA释放和PLA₂的基因表达。