模拟失重增强大鼠脑动脉血管平滑肌细胞大电导钙激活钾通道功能

本工作旨在探讨短期模拟失重大鼠脑动脉血管平滑肌细胞（vascular smooth muscle cells,VSMCs）大电导钙激活钾通道（large conductance calcium-activated potassium channels,BKCa channels）功能的改变。以尾部悬吊大鼠模型模拟失重对脑血管的影响。应用激光扫描共聚焦显微镜测定VSMCs胞内游离钙浓度（[Ca^2＋]i）;采用细胞贴附模式,记录BKCa通道的单通道活动。结果表明,模拟失重1周后,大鼠脑动脉VSMCs的[Ca^2＋]i比对照组显著升高（P〈0．05）：BKCa通道的开放概率（Po）与平均开放时间（To）显著增加（P〈0．05）,而单通道电导与平均关闭时间（Tc）则无显著变化。总之,1周模拟失重可引起脑动脉VSMCs的BKCa通道功能显著增强,且与细胞[Ca^2＋]i的升高同步出现。结果提示,脑动脉VSMCs的离子通道机制可能参与介导模拟失重引起的脑血管适应性变化。     

尼古丁调节大鼠冠状动脉平滑肌细胞大电导钙激活钾通道

目的:研究尼古丁对Wistar大鼠冠状动脉平滑肌大电导钙激活钾通道(BKca)活性的抑制作用及其细胞信号转导机制。方法:8周雄性Wistar大鼠随机分为两组:生理盐水组和尼古丁组;分别予以生理盐水和尼古丁2mg/(kg.d)注射21 d,蛋白酶法分离冠状动脉血管平滑肌细胞,将两组平滑肌细胞分别以对氯苯硫基环腺苷酸(CPT-cAMP,100μmol/L)和佛司可林(forskolin,10μmol/L)干预,单通道膜片钳记录干预前后平滑肌细胞单通道电流的平均开放时间(To)、平均关闭时间(Tc)、平均开放概率(Po)。结果:CPT-cAMP和Forskolin均能显著延长生理盐水组大鼠BKca的平均开放时间,缩短平均关闭时间,增加通道开放概率(P均<0.01)。对尼古丁组BKca的To、Tc、Po均无明显影响。结论:尼古丁促使冠状动脉血管收缩的生理机制是通过抑制cAMP/PKA途径诱导的大电导钙激活钾通道活性增加实现的。     

外源褪黑素调控棉花枯萎病抗性研究

为探究外源褪黑素对棉花抗枯萎病的影响及作用机理,以海岛棉新海14号为材料,于叶面喷施不同浓度褪黑素（0、10、25、50、75、100 μmol/L）后接种棉花枯萎病菌,对枯萎病菌侵染后棉花幼苗进行抗病性鉴定、抗病相关酶活性及基因表达分析。结果表明,外源褪黑素对棉花枯萎病菌的生长无抑制作用,10-100 μmol/L褪黑素均能在一定程度上提高棉花对枯萎病的抗性,其中50 μmol/L褪黑素处理效果最好。与对照相比,50 μmol/L褪黑素预处理能有效减少接菌后棉花叶片中的过氧化氢（H₂O₂）含量和超氧阴离子（O₂^·-）的产生速率,增强过氧化物酶（POD）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、抗坏血酸过氧化物酶（APX）、几丁质酶（CHT）、β-1,3葡聚糖酶（GLU）、多酚氧化酶（PPO）、苯丙氨酸解氨酶（PAL）活性,并显著提高木质素代谢途径相关基因（GbPAL、Gb4CL和GbCAD）和类黄酮代谢途径关键基因（GbCHI、GbDFR和GbTT7）的表达量。表明50 μmol/L 的褪黑素处理能提高接菌后棉花抗氧化能力,增强防御酶活性,调控木质素、类黄酮代谢途径相关基因的表达,从而提高棉花对枯萎病的抗性。     

NaHS对ATP诱导大鼠小胶质细胞P2X受体表达的影响

目的：观察硫化氢（H₂S）供体硫氢化钠（NaHS）对ATP致伤的大鼠小胶质细胞细胞活力、细胞膜通透性及P2X7受体表达的影响。方法：实验取对数期形态结构及生长分化良好的大鼠小胶质细胞,随机分4组,每组设3个复孔。①正常对照组：常规培养,不进行ATP处理。②ATP组：接种细胞24 h后ATP处理。③NaHS+ATP组：NaHS预先孵育30 min后再用ATP处理,并且NaHS始终存在于反应体系中。④KN-62（P2X₇受体阻断剂）+ATP组：KN-62预先孵育30 min,其余同NaHS+ATP组。MTT检测各组细胞活力,荧光染料YO-PRO-1检测各组相对荧光单位（RFU）反映膜的通透性,Western blot检测各组P2X₇受体表达水平。结果：①与对照组相比,不同浓度的ATP （1、3、5、10 mmol/L）作用3 h均可明显降低大鼠小胶质细胞活力,NaHS （200 μmol/L）干预后大鼠小胶质细胞活力较ATP组明显增加（P<0.01）,但NaHS达400 μmol/L浓度时,其保护作用未进一步增加。②随着ATP浓度的增加,大鼠小胶质细胞内YO-PRO-1的荧光强度显著增加,NaHS预处理可明显减少细胞对YO-PRO-1的摄取（P<0.01）。③ATP （3 mmol/L）能上调P2X₇受体蛋白表达水平,而NaHS （200 μmol/L）预孵育则可明显抑制ATP引起的P2X₇受体蛋白表达的上调（P<0.01）。结论：NaHS可减少ATP致伤的大鼠小胶质细胞的P2X₇受体表达、降低通透性、增加细胞活力,提示调控P2X₇受体的表达和功能可能是H₂S神经保护作用的重要环节。     

高血压病患者肠系膜动脉平滑肌细胞钙激活钾通道研究

目的:研究高血压病患者肠系膜动脉平滑肌细胞钙激活钾通道(KCa)的功能活动。方法:应用膜片钳制技术内面向外式单通道记录方法。结果:①人肠系膜动脉平滑肌细胞KCa开放具有电压依赖性。KCa通道电导在高血压组、正常组分别为191.4pS、197.7pS。胞内侧应用TEA可阻断通道。②增加浴液中Ca2 浓度(从0增至10-8、10-7、5×10-7、10-6mol/L),各组KCa开放概率(Po)均呈浓度依赖性增加,高血压组Po从0.016增至0.023、0.031、0.053、0.094,正常组Po从0.004增至0.023、0.041、0.072、0.184。通道平均开放时间延长,平均关闭时间缩短。③Ca2 浓度为0时,高血压组KCa开放概率明显高于正常组,在其它Ca2 浓度下高血压组KCa开放概率等于或低于正常组。结论:高血压病患者肠系膜动脉平滑肌细胞KCa的Ca2 敏感性较低,可能促进高血压的发生。     

Flag和GFP双标记的BKCa通道α亚基表达质粒的构建、鉴定和序列分析

目的：采用重叠PCR法构建表达质粒,为下一步研究通道功能奠定基础。方法：在已有编码大电导钙激活钾通道（BK_Ca）通道α亚单位的表达质粒pcDNA3.1-hSlo的基础上,采用重叠PCR法构建Flag和GFP双标签标记的表达质粒pcDNA3.1-Flag-hSlo-GFP （Flag-hSlo-GFP）。结果：构建的表达质粒Flag标签插入BK_Ca通道的S1-S2胞外环,GFP标签连接BK_Ca通道的胞内C末端,测序结果证实质粒构建成功。结论：成功构建BK通道基因表达质粒Flag-hSlo-GFP,重叠PCR能够很好的用于长片段基因扩增和插入片段的实验。     

钙激活钾通道在黎芦碱致神经细胞损伤中的作用

目的:观察新生SD大鼠原代培养皮层神经元的钙激活钾通道(Kca)在黎芦碱致神经元损伤模型上的激活、抑制效应.方法:采用细胞贴附和内面向外两种膜片钳单通道记录方法记录新生SD大鼠原代培养皮层神经元的Kca电生理活动.结果:黎芦碱在胞外可激活Kca.在有钙浴液内,细胞贴附式,钳制膜电位 30 mV,加入不同浓度黎芦碱(μmol/L:15、25、50、75),通道开放概率由0.005分别增加为0.014±0.003、0.085±0.010、0.132±0.016、0.059±0.006(P＜0.01),在50μmol/L以内表现出浓度依赖性.无钙浴液内,细胞贴附式膜片上,钳制膜电位 50 mV,随药物浓度(μmol/L)增加为15、40、60、100时,通道开放概率由0.005分别增加为0.014±0.010、0.113±0.006、0.141±0.004、0 295±0.009(P＜0.05).6例内面向外式膜片上,钳制膜电位 40 mV,分别加入黎芦碱25 μmol/L、50μmol/L 3 min后,通道开放概率由0.011±0.008分别增加为0.010±0.010、0.012±0.007(P＞0.05).黎芦碱在胞内Kca开放概率,平均开放/关闭时间,电流幅值均无明显变化.结论:黎芦碱通过影响胞内游离钙水平间接调节Kca,在缺血缺氧早期,胞内游离钙增高激活Kca开放.     

氯通道在葛根素注射液致溶血反应中的作用

目的：观察阻断和激活氯通道对葛根素注射液致家兔溶血反应的影响,探讨氯通道在葛根素注射液溶血反应中的作用。方法：将不同浓度的葛根素注射液（0.75、1.5、3、6、12 mg/ml）与家兔红细胞悬液共孵育6 h,使用细胞图像记录系统观测葛根素注射液是否诱导红细胞溶血,酶标仪、流式细胞仪检测红细胞溶血率,并观测激活和阻断氯通道对葛根素注射液溶血作用的影响。结果：葛根素注射液可引起家兔红细胞体外溶血,在所观察的1.5 mg/ml~12 mg/ml范围内,溶血效应呈浓度依赖性增强（n=3,P<0.01）。氯通道阻断剂Tamoxifen （20 μmol/L）、ATP （10 mmol/L）可有效抑制葛根素注射液的溶血作用（n=3~5,P<0.01）;而使用低浓度ATP （50 μmol/L）激活氯通道,则显著增强葛根素注射液的溶血作用（n=4,P<0.01）。结论：葛根素注射液的体外溶血效应呈浓度依赖性,氯通道激活与葛根素注射液诱导的溶血反应密切相关。     

心房肌胞内钙浓度变化对心房颤动患者小电导钙激活钾通道电流的影响

目的：SK通道存在于心肌细胞上,其中SK2亚型主要表达在心房。SK2通道对胞内游离钙离子高度敏感,可快速将钙离子浓度的变化转换成细胞膜电位变化。本实验应用穿孔膜片钳技术记录人心肌细胞SK2电流,观察心房肌细胞SK2电流在窦性患者和心房颤动患者之间的差别,以及电极液中不同的钙浓度对两组细胞SK2电流的影响。方法：将接受体外循环手术的患者分为两组：心房颤动组和窦性心律组。以心房肌细胞为研究对象,用穿孔膜片钳技术记录人心肌细胞电流,观察窦性组与房颤组SK2通道电流的差异以及两组细胞SK2电流对电极液中钙敏感性的不同。结果：在全细胞穿孔膜片钳模式下,电极液中游离钙离子浓度为5×10-7mol/L时,记录到房颤组SK2通道电流明显大于窦性组,尤其是在超极化水平。膜电位在-130 mV时,窦性组与房颤组的SK2通道电流密度分别为（-2.92±0.35）pA/pF（n=6）,（-6.83±0.19）pA/pF（n=3,P〈0.05）。在电极液游离钙离子浓度分别为0 mol/L、5×10-7mol/L、10-6mol/L,膜电位为-130 mV时,窦性组SK2通道电流密度分别为（-1.43±0.33）pA/pF（n=7）,（-2.92±0.35）pA/pF（n=6）,（-10.11±2.15）pA/pF（n=8,P〈0.05）;房颤组SK2通道电流密度分别为（-2.17±0.40）pA/pF（n=4）（-6.83±0.19）pA/pF（n=3）（-14.47±2.89）pA/pF（n=4）（P〈0.05）。结论：人心房肌细胞SK2通道具有电压不敏感、内向整流、apamin敏感的特性。电极液中钙浓度相同的情况下,房颤组的SK2电流密度明显大于窦性组,SK2通道电流对钙离子的敏感性高于窦性组,提示SK2通道钙敏感性增加可能与心房颤动的发生发展密切相关。     

常温和低温条件下不同浓度外源褪黑素对降香黄檀幼苗的生理生态影响

为探究外源褪黑素对不同温度下降香黄檀幼苗的生理生态影响,该研究开展了不同浓度外源褪黑素(300、500、600、700、900、1 200μmol·L^-1)对常温（白天28℃/夜晚25℃）和低温（白天8℃/夜晚5℃）下降香黄檀（Dalbergia odorifera）幼苗的生长发育、光合作用、叶片色素含量、叶片水分状况、膜系统等方面影响研究,并通过隶属函数分析综合评价筛选出具有促进降香黄檀幼苗生长发育和提高低温耐受性的最适外源褪黑素浓度。结果表明：（1）在常温下喷施各个浓度的褪黑素溶液,在生长发育（形态、茎高增长和株高增长）,光合作用参数[净光合速率（P_n）、气孔导度（G_s）、胞间二氧化碳浓度（C_i）和蒸腾速率（T_r）],光合色素[总叶绿素（Total Chl）、叶绿素a（Chl a）、叶绿素b（Chl b）和类胡萝卜素（Caro）]和可溶性蛋白含量上均有一定的提高。（2）低温胁迫处理下,喷施各个浓度的褪黑素溶液可在不同程度上缓解低温胁迫对植株形态、茎高增长、株高增长、P     

Melatonin synchronizes protein synthesis rhythm in hepatocyte cultures as an agonist of intercellular calcium and protein kinases

Melatonin in nanomolar concentrations synchronizes protein synthesis in primary cultures of hepatocytes through calcium-dependent activation of protein kinases. The synchronizing effect of melatonin is blocked by the cytoplasmic calcium chelating agent BAPTA-AM (20 μM) as well as by the inhibitor of protein kinases 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (40 μM). Thus, protein phosphorylation is the key event in hepatocyte synchronization by melatonin, as we have demonstrated previously for gangliosides and biogenic amines. The antagonist of melatonin receptors luzindole (20 nM) blocks the synchronizing function of melatonin.     

Multiple binding sites for melatonin on Kv1.3

Melatonin is a small amino acid derivative hormone of the pineal gland. Melatonin quickly and reversibly blocked Kv1.3 channels, the predominant voltage-gated potassium channel in human T-lymphocytes, acting from the extracellular side. The block did not show state or voltage dependence and was associated with an increased inactivation rate of the current. A half-blocking concentration of 1.5 mM was obtained from the reduction of the peak current. We explored several models to describe the stoichiometry of melatonin-Kv1.3 interaction considering one or four independent binding sites per channel. The model in which the occupancy of one of four binding sites by melatonin is sufficient to block the channels gives the best fit to the dose-response relationship, although all four binding sites can be occupied by the drug. The dissociation constant for the individual binding sites is 8.11 mM. Parallel application of charybdotoxin and melatonin showed that both compounds can simultaneously bind to the channels, thereby localizing the melatonin binding site out of the pore region. However, binding of tetraethylammonium to its receptor decreases the melatonin affinity, and vice versa. Thus, the occupancy of the two separate receptor sites allosterically modulates each other.     

Effects of the blockade of high voltage-activated calcium channels on in vitro pineal melatonin synthesis

The presence of high voltage-activated calcium channels in the rat pineal gland is well known. However, their role in pineal metabolism is not completely understood and is even controversial. Better to understand this matter, we investigated the effects of L-, N- or P/Q-type calcium channel blockers (nifedipine, omega-conotoxin GVIA, omega-agatoxin IVA, respectively) on melatonin content and arylalkylamine-N-acetyltransferase activity of denervated rat pineal glands kept for 48 h in culture and stimulated with norepinephrine. Melatonin was measured by high performance liquid chromatography with electrochemical detection and arylalkylamine-N-acetyltransferase activity was quantified by radiometric assay. Pre-incubation with any of these high voltage-activated calcium channel blockers reduced the melatonin production induced by norepinephrine although arylalkylamine-N-acetyltransferase activity was reduced only by the N-type calcium channel antagonist, omega-conotoxin GVIA. The results indicate that calcium influx through L-, N- or P/Q-type of high voltage-activated calcium channels is necessary for the full expression of the metabolic process leading to melatonin synthesis in the rat pineal glands. However, the mechanisms involved in this process are different for the L- or P/Q- and N-type calcium channels.     

Melatonin reduces cerebral edema formation caused by transient forebrain ischemia in rats

Reduction of cerebral edema, an early symptom of ischemia, is one of the most important remedies for reducing subsequent chronic neural damage in stroke. Melatonin, a metabolite of tryptophan released from the pineal gland, has been found to be effective against neurotoxicity in vitro. The present study was aimed to demonstrate the effectiveness of melatonin in vivo in reducing ischemia-induced edema using magnetic resonance imaging (MRI). Rats were subjected to middle cerebral artery (MCA) occlusion/reperfusion surgery. Melatonin was administered twice (6.0 mg/kg, p.o.): just prior to 1 h MCA occlusion and 1 day after the surgery. T2-weighted multislice spin-echo images were acquired 1 day after the surgery. Increases in T2-weighted signals in ischemic sites of the brain were clearly observed after MCA occlusion. The signal increase was found mainly in the striatum and in the cerebral cortex in saline-treated control rats. In the melatonin-treated group, the total volume of cerebral edema was reduced by 45.3% compared to control group (P < 0.01). The protective effect of melatonin against cerebral edema was more clearly observed in the cerebral cortex (reduced by 56.1%, P < 0.01), while the reduction of edema volume in the striatum was weak (reduced by 23.0%). The present MRI study clearly demonstrated that melatonin is effective in reducing edema formation in ischemic animals in vivo, especially in the cerebral cortex. Melatonin may be highly useful in preventing cortical dysfunctions such as motor, sensory, memory, and psychological impairments.     

川芎嗪对猪冠状动脉平滑肌细胞大电导钙激活钾通道的作用

本工作旨在研究川芎嗪对猪冠状动脉平滑肌细胞钾通道的作用,为阐明其扩张冠状动脉血管的机制提供实验依据。采用膜片钳细胞贴附式和内面向外式记录方式观察川芎嗪对猪冠状动脉平滑肌细胞大电导钙激活钾通道(large-conductance Ca2+- activated potassium channels,BKCa channels)的作用,分别用蛋白激酶A(protein kinase A,PKA)抑制剂H-89和蛋白激酶G (protein kinase G,PKG)抑制剂KT-5823处理细胞,再观察川芎嗪对BKCa通道作用的变化。结果表明在研究的0．73-8．07 mmol/L浓度范围,川芎嗪可以剂量依赖性地激活BKCa通道,使通道的开放概率从(0．01±0．003)增加到(0．03±0．01)-(．21± 0．18)(P<0．01,n=10),使通道平均关闭时间从(732．33±90．67)ms降低到(359．67±41．30)-(2．96±0．52)ms(P<0．01, n=10)。川芎嗪的这种激活作用在浴液游离钙离子浓度接近0 mmol/L时也存在。PKA的特异性抑制剂H-89(3 μmol/L)和 PKG的特异性抑制剂KT-5823(1 μmol/L)对川芎嗪激活BKCa通道的作用无影响。以上结果提示:川芎嗪能直接激活冠状动脉平滑肌BKCa通道,这种作用可能是川芎嗪扩张冠状动脉血管的一种重要机制。     

Melatonin ameliorates neural function by promoting endogenous neurogenesis through the MT2 melatonin receptor in ischemic-stroke mice

Melatonin has many protective effects against ischemic stroke, but the underlying neuroprotective mechanisms are not fully understood. Our aim was to explore the relationship between melatonin's neuroprotective effects and activation of the MT2 melatonin receptor in a murine ischemic-stroke model. Male ICR mice were subjected to a transient middle cerebral ischemic/reperfusional injury, and melatonin (5 and 10 mg/kg, ip) was administrated once daily starting 2 h after ischemia. More than 80% of the mice died within 5 days after stroke without treatment. Melatonin treatment significantly improved the survival rates and neural functioning with modestly prolonged life span of the stroke mice by preserving blood-brain barrier (BBB) integrity via a reduction in the enormous amount of stroke-induced free radical production and significant gp91(phox) cell infiltration. These protective effects of melatonin were reversed by pretreatment with MT2 melatonin receptor antagonists (4-phenyl-2-propionamidotetralin (4P-PDOT) and luzindole). Moreover, treatment with melatonin after stroke dramatically enhanced endogenous neurogenesis (doublecortin positive) and cell proliferation (ki67 positive) in the peri-infarct regions. Most ki67-positive cells were nestin-positive and NG2-positive neural stem/progenitor cells that coexpressed two neurodevelopmental proteins (adam11 and adamts20) and the MT2 melatonin receptor. RT-PCR revealed that the gene expression levels of doublecortin, ki67, adamts20, and adam11 are markedly reduced by stroke, but are restored by melatonin treatment; furthermore, pretreatment with 4P-PDOT and luzindole antagonized melatonin's restorative effect. Our results support the hypothesis that melatonin is able to protect mice against stroke by activating MT2 melatonin receptors, which reduces oxidative/inflammatory stress. This results in the preservation of BBB integrity and enhances endogenous neurogenesis by upregulating neurodevelopmental gene/protein expression.     

Melatonin receptor signaling in pregnant and nonpregnant rat uterine myocytes as probed by large conductance Ca2+-activated K+ channel activity

The mRNAs of MT1 and MT2 melatonin receptors are present in cells from nonpregnant (NPM) and pregnant (PM) rat myometrium. To investigate the coupling of melatonin receptors to Gq- and Gi-type of heterotrimeric G proteins, we analyzed the activity of large-conductance Ca2+-activated K+ (BKCa) channels, the expression of which in the uterus is confined to smooth muscle cells. The melatonin receptor agonist 2-iodomelatonin induced a pertussis toxin (PTX)-insensitive increase in channel open probability that was blocked by the nonselective antagonist luzindole. The 2-iodomelatonin effect on channel open probability was suppressed by overexpression of the Gqalpha-inactivating protein RGS16 and the phospholipase C inhibitor U-73122. The activity of BKCa channels is differentially regulated by protein kinase A (PKA) in NPM and PM cells. Thus, the beta-adrenoceptor agonist isoprenaline inhibited the BKCa channel conducted whole-cell outward current (Iout) in NPM cells and enhanced Iout in PM cells. Additional application of 2-iodomelatonin antagonized the isoprenaline effect on Iout in NPM cells but enhanced Iout in PM cells. All 2-iodomelatonin effects on Iout were sensitive to PTX treatment and the PKA inhibitor H-89. We therefore conclude that melatonin activates both the PTX-insensitive Gq/phospholipase C/Ca2+ and the PTX-sensitive Gi/cAMP/PKA signaling pathway in rat myometrium.     

Glial cell survival is enhanced during melatonin-induced neuroprotection against cerebral ischemia.

The role of glial cells in neuronal death has become a major research interest. Glial cell activation has been demonstrated to accompany cerebral ischemia. However, there is disagreement whether such gliosis is a cell death or a neuroprotective response. In the present study, we examined alterations in glial cell responses to the reported neuroprotective action of the free radical scavenger, melatonin, against cerebral ischemia. Adult male Wistar rats were given oral injections of either melatonin (26 micromol/rat) or saline just prior to 1 h occlusion of the middle cerebral artery (MCA), then once daily for 11 or 19 consecutive days. At 11 and 19 days after reperfusion of the MCA, randomly selected animals were killed and their brains removed for immunohistochemical assays. Melatonin significantly enhanced survival of glial cells (as revealed by glial cell specific markers, glial fibrillary acidic protein and aquaporin-4 immunostaining) at both time periods postischemia, and the preservation of these glial cells in the ischemic penumbra corresponded with a markedly reduced area of infarction (detected by immunoglobulin G and hematoxylin-eosin staining), as well as increased neuronal survival. The ischemia-induced locomotor deficits were partially ameliorated in melatonin-treated animals. In vitro replications of ischemia by serum deprivation or by exposure to free radical-producing toxins (sodium nitroprusside and 3-nitropropionic acid) revealed that melatonin (10 microg/ml or 100 microM) treatment of pure astrocytic cultures significantly reduced astrocytic cell death. These results suggest a potential strategy directed at enhancing glial cell survival as an alternative protective approach against ischemic damage.     

Melatonin Promotes Rice Seed Germination under Drought Stress by Regulating Antioxidant Capacity

Drought stress is a serious threat to the germination of plant seeds and the growth of seedlings. Melatonin has been proven to play an important role in alleviating plant stress. However, its effect on seed germination under drought conditions is still poorly understood. Therefore, we studied the effects of melatonin on rice seed germination and physiological characteristics under drought stress. Rice seeds were treated with different concentrations of melatonin (i.e., 0, 20, 100, and 500 μM) and drought stress was simulated with 5% polyethylene glycol 6000 (PEG6000). The results showed that 100 μM melatonin can effectively improve the germination potential, rate and index; the vigor index of rice seeds; and the length of the shoot and root. In addition, that treatment also increased the activity of superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT), and reduced the content of malondialdehyde (MDA). The grey relational grade between the shoot MDA content and the melatonin seed-soaking treatment was the highest, which could be useful for evaluating the effect of melatonin on drought tolerance. Two-way analysis of variance showed that the effect of single melatonin treatment on rice seeds was more significant than that of single drought stress and interaction treatment of drought and melatonin (p < 0.05). The subordinate function results showed that 100 μM melatonin significantly improved the germination and physiological indexes of rice seeds and effectively alleviated the adverse effects of drought stress on rice seedlings. The results helped to improve the understanding of the morphological and physiological involvement of melatonin in promoting seed germination and seedling development under drought stress.