黄芩苷磷脂复合物抗炎时效初步研究

目的比较黄芩苷、黄芩苷磷脂复合物的抗炎时效关系。方法制备黄芩苷磷脂复合物;用二甲苯致小鼠腹部皮肤毛细血管通透性亢进炎症模型和耳肿模型;分光光度法测定腹部蓝染皮肤伊文思蓝渗出量。结果抗炎时效曲线显示黄芩苷磷脂复合物组小鼠腹部皮肤伊文思蓝的渗出量在0.5 h即与对照组有显著差异,而黄芩苷则发生在1 h左右。磷脂复合物组3 h抗炎作用达到最强,21 h内均呈现出明显的抗炎作用。而黄芩苷组在4 h时抗炎作用最大,之后抗炎作用下降,16 h后已无作用。黄芩苷组与黄芩苷磷脂复合物组在给药后2 h抗炎作用已经表现出显著的差异,磷脂复合物组强于黄芩苷组。结论黄芩苷磷脂复合物的抗炎活性明显强于黄芩苷,且作用出现更迅速、维持时间更久。     

黄芩苷磷脂复合物抗炎时效初步研究

目的比较黄芩苷、黄芩苷磷脂复合物的抗炎时效关系。方法制备黄芩苷磷脂复合物;用二甲苯致小鼠腹部皮肤毛细血管通透性亢进炎症模型和耳肿模型;分光光度法测定腹部蓝染皮肤伊文思蓝渗出量。结果抗炎时效曲线显示黄芩苷磷脂复合物组小鼠腹部皮肤伊文思蓝的渗出量在0.5 h即与对照组有显著差异,而黄芩苷则发生在1 h左右。磷脂复合物组3 h抗炎作用达到最强,21 h内均呈现出明显的抗炎作用。而黄芩苷组在4 h时抗炎作用最大,之后抗炎作用下降,16 h后已无作用。黄芩苷组与黄芩苷磷脂复合物组在给药后2 h抗炎作用已经表现出显著的差异,磷脂复合物组强于黄芩苷组。结论黄芩苷磷脂复合物的抗炎活性明显强于黄芩苷,且作用出现更迅速、维持时间更久。     

红曲抗炎作用的实验研究

目的：研究红曲的抗炎作用。方法：急性抗炎模型采用巴豆油致小鼠耳肿胀模型和角叉菜胶致大鼠足肿胀模型，慢性抗炎模型采用棉球植入小鼠腹腔致肉芽肿模型。以布洛芬作阳性对照，并设洛伐他汀高、低剂量组。比较红曲与洛伐他汀的抗炎作用。结果：红曲对巴豆油致小鼠耳肿胀、角叉菜胶致大鼠足肿胀和棉球致小鼠腹腔肉芽肿均有显著的抑制作用，与洛伐他汀的抗炎作用相近。结论：红曲具有显著的抗炎作用。     

小檗碱抗炎活性研究

目的观察小檗碱的抗炎作用。方法采用甲醛致小鼠足肿胀法观察小檗碱对炎症局部组织中前列腺素(PGE2)的影响。结果小檗碱能显著降低炎性组织中PGE2的含量。结论小檗碱具有明显抗炎作用,其机制与抑制组织中PGE2生成有关。     

川黄柏抗炎活性部位的筛选研究

目的 研究川黄柏提取物的抗炎效果.方法 采用二甲苯致小鼠耳廓肿胀、1％冰乙酸致小鼠腹腔毛细血管通透性模型、鸡蛋清诱导大鼠足跖肿胀和大鼠肿胀足炎性组织中PGE2的影响等急性炎症模型,观察川黄柏提取物的抗炎作用.结果 川黄柏提取物对4种急性炎症模型均有不同程度的抑制作用,其中,生物碱部位与模型组比较有显著性差异.结论 川黄柏提取物的生物碱部分具有良好的抗炎作用,其他各部位也具有不同强度的抗炎作用.     

牡荆素的镇痛及抗炎免疫作用研究

目的旨在探讨牡荆素镇痛作用和抗炎免疫调节作用的机制。方法应用热板法测定痛阈值,以研究牡荆素的镇痛效果。通过对角叉菜胶诱发大鼠足趾肿胀试验,来观察牡荆素抗炎作用;利用醋酸影响小鼠腹腔毛细血管通透性的方法,观察牡荆素的免疫清除作用。结果牡荆素大剂量组痛阈提高值的百分率(%)最大达(40.3±14.8),比同期对照组的(5.9±1.8)有显著差异(P<0.01);和模型组比较,牡荆素各剂量组在致炎后1、2、3、5 h均有不同程度的足趾肿胀抑制(P<0.05),其中牡荆素大剂量组大鼠(200 mg/kg)在致炎后1 h开始到3 h达到最高值(45.3±14.8);与对照组比较差异更为显著(P<0.01);与对照组比较,牡荆素大剂量组对小鼠腹腔毛细血管通透性的吸收度A明显低于对照组,差异有显著性意义(P<0.01)。结论牡荆素具有较好的镇痛效果,抗炎作用明显;并能明显增强小鼠腹腔巨噬细胞的吞噬能力。     

紫杉醇脂质体凝胶剂的制备及其镇痛抗炎作用

目的制备紫杉醇脂质体凝胶剂,对其镇痛抗炎作用进行初步研究。方法薄膜分散法制备紫杉醇脂质体,用透射电镜观测其形态,用激光纳米粒度仪测定粒径大小及分布,用HPLC测定其包封率。脂质体进一步制成凝胶剂后,体外透皮实验测定其不同时间的体外透皮量,考察其体外透皮情况。大鼠角叉菜胶致足肿胀模型及小鼠甲醛致痛模型,考察紫杉醇脂质体凝胶剂的镇痛抗炎作用。结果制得的紫杉醇脂质体形态规则、分布均匀,平均包封率为(73.6±0.3)%(n=3),所得凝胶呈半透明状;体外透皮实验中,紫杉醇脂质体凝胶剂符合一级动力学方程,起到较好的缓释作用。抗炎实验中,与模型组比较,各给药组在一定时间内均能显著性减轻致炎足趾的肿胀程度(P<0.05),并呈现明显的量效关系。甲醛致痛实验中,给药组与模型组比较,小鼠舔足次数明显减少(P<0.05)。结论紫杉醇脂质体凝胶具有明显镇痛抗炎作用。     

3种他汀类药物抗炎作用的实验研究

目的:研究3种他汀类药物的抗炎作用.方法:急性抗炎模型采用巴豆油致小鼠耳肿胀模型和角叉菜胶致大鼠足肿胀模型,慢性抗炎模型采用棉球植入小鼠腹腔致肉芽肿模型.以布洛芬作为阳性对照,观察洛伐他汀、辛伐他汀和普伐他汀的抗炎作用.结果:他汀类药物对巴豆油致小鼠耳肿胀、角叉菜胶致大鼠足肿胀和棉球致小鼠腹腔肉芽肿形成均有显著的抑制作用.结论:他汀类药物具有显著的抗炎作用.     

不同时间配制的角叉菜胶致大鼠足爪肿作用比较

角叉菜胶致大鼠足爪肿模型是研究抗炎药物的常用方法。部分作者主张,致肿剂应于用前24h配制,否则影响致肿效果,但缺乏实验依据。本文应用24h或1wk前配制的角叉菜胶进行比较,二者对大鼠后足容积变化百分率的趋势及峰值均无显著差异(p>0.05);所致足肿胀对水杨酸钠300mg/kg,ip的抗炎作用亦无明显差异(p>0.5),此抗炎作用与NS ip对照组比较,抑肿作用显著(p<0.01)。     

银黄方膜分离物解热抗炎作用的研究

目的在膜分离工艺和有效成分研究的基础上,对银黄方膜分离物的解热抗炎作用进行研究,以了解膜分离工艺的物质基础对银黄方相关药效的影响。方法以解热、抗炎为主要药效学指标,观察银黄方对鲜酵母致大鼠体温升高的抑制作用,对羧甲基纤维素钠致小鼠白细胞游出抗炎作用。结果银黄方膜分离物第三、四、五级膜分离物的降温作用出现在致热后的3h,降温作用持续2h,均与模型组比较差异显著(P<0.01,P<0.001);银黄方膜分离物第三、四、五级组小鼠白细胞游出数量明显减少,与模型组比较差异显著(P<0.05,P<0.01)。结论银黄方膜分离物具有解热及抗炎作用,进一步证明了膜分离技术应用于中药复方有效成分或有效部位的分离富集的可行性。     

Efficacy of bufexamac cream versus betamethasone valerate cream in contact dermatitis: a double-blind trial.

A double-blind controlled study was carried out in 72 patients with atopic or contact dermatitis, who were randomly allocated to receive treatment with either 5% bufexamac, 0.1% betamethasone valerate or placebo creams. Patients applied the cream twice daily for 2 weeks. Assessments of the degree of severity of inflammation, induration, lichenification, crusts, scaling, and pruritus were made before and after treatment. The results showed that both active preparations were equally effective in improving the skin condition in the majority of the patients. In younger patients, however, the improvement with betamethasone valerate appeared to be somewhat better than that with bufexamac, particularly in relation to pruritus.     

Efficacy of bufexamac cream versus betamethasone valerate cream in contact dermatitis: a double-blind trial

Summary

A double-blind controlled study was carried out in 72 patients with atopic or contact dermatitis, who were randomly allocated to receive treatment with either 5% bufexamac, 0.1% betamethasone valerate or placebo creams. Patients applied the cream twice daily for 2 weeks. Assessments of the degree of severity of inflammation, induration, lichenification, crusts, scaling, and pruritus were made before and after treatment. The results showed that both active preparations were equally effective in improving the skin condition in the majority of the patients. In younger patients, however, the improvement with betamethasone valerate appeared to be somewhat better than that with bufexamac, particularly in relation to pruritus.     

Anti-inflammatory and skin-hydrating properties of a dietary supplement and topical formulations containing oligomeric proanthocyanidins

BACKGROUND: Anti-inflammatory and skin hydration properties of a dietary supplement and 2 topical formulations (Anthogenol) with oligomeric proanthocyanidins were investigated. METHODS: Forty-two subjects were randomized into 2 groups: one taking the dietary supplement (100 mg/day) and the other without supplement. After 4 weeks, erythema was induced using UV radiation followed by treatment with topical cream or lotion. Erythema was measured for up to 72 h after irradiation. Skin hydration after 1 and 2 weeks of application of the cream and lotion was also measured in separate test fields. RESULTS: Both topical formulations led to a significant suppression of erythema formation and the dietary supplement led to an additional slightly stronger suppression. Thus 72 h after UV exposure and compared to the control fields of patients that had not taken a dietary supplement, erythema was slightly (13.2%) lower in the subjects that had taken a dietary supplement. The cream resulted in a maximal reduction of erythema of 45.9% (p = 0.0015), while the lotion resulted in a maximal reduction of 53.1% (p = 0.0002). Both topical formulations also increased skin hydration (by nearly 20%; p < 0.002 for all combinations of dietary supplementation and topical treatment) and the hydration was higher in the group taking the dietary supplement. CONCLUSION: The regular use of Anthogenol products may help to protect from free-radical-mediated skin inflammation and to increase skin hydration.     

A novel treatment of contact dermatitis by topical application of phospholipase A2 inhibitor: a double-blind placebo-controlled pilot study

Phospholipase A2 hydrolyzes membrane phospholipids releasing arachidonic acid and lysophospholipids. These are key precursors of inflammatory mediators, such as prostaglandins, leukotrienes, thromboxanes and PAF, in numerous inflammatory/allergic diseases, including skin inflammation. Accordingly, inhibition of PLA2 has long been postulated as a potentially potent anti-inflammatory therapy. In the present study we tested the effect of a novel PLA2 inhibitor on contact dermatitis in human subjects. A double-blind, placebo-controlled pilot study was conducted on contact dermatitis patients (n = 11) treated with the inhibitor-containing topical preparation (1% cream). Disease severity was assessed by physicians assessment before treatment (day 0) as well as after 14-days and 30-days. Patients treated with 1% PLA2 inhibitor-containing cream showed a 69.9% reduction in disease score while placebo-treated patients showed a reduction of 36.5% with p = 0.0024. The clear improvement in the disease score of inhibitor-treated patients supports the involvement of PLA2 activity in skin inflammation and the therapeutic prospective of its inhibition.     

Effect of a 5-lipoxygenase (5-LO)/cyclooxygenase (CO) inhibitor, WY-47, 288, on cutaneous models of inflammation

WY-47,288 (2-[(1-naphthalenyloxy)methyl]quinoline) demonstrated topical antiinflammatory activity in several animal models of skin inflammation. Application of WY-47,288 to mouse ear surfaces inhibited arachidonic acid (ED50 = 0.3 mg/ear) and tetradecanoylphorbol acetate (TPA)-induced inflammation (40% at 1 mg/ear). Administration of WY-47,288 (1 mg/ear) at 30 min and 5 h after TPA reduced ear edema and epidermal proliferation by 50%. WY-47,288 also inhibited oxazolone-induced contact hypersensitivity in mouse ears (ED50 = 0.4 mg/ear) and UVB-induced guinea pig skin erythema (ED50 approximately 0.25 mg/spot). These antiinflammatory effects may be due to inhibition of 5-lipoxygenase (5-LO) and cyclooxygenase (CO) since the synthesis of 5-LO and CO products by rat neutrophils and mouse macrophages was dose-dependently reduced by WY-47,288. By contrast, WY-47,288 demonstrated no appreciable inhibition of 12-LO (rabbit platelet), 15-LO (soybean) or phospholipase A2 (human platelet). Furthermore, no systemic adverse effects were observed after topical, parenteral or oral administration of WY-47,288, suggesting that WY-47,288 is a safe topical 5-LO/CO inhibitor for treating skin inflammation.     

The phosphodiesterase 4 inhibitor AWD 12-281 is active in a new guinea-pig model of allergic skin inflammation predictive of human skin penetration and suppresses both Th1 and Th2 cytokines in mice

The selective phosphodiesterase 4 (PDE4) inhibitor AWD 12-281 is structurally optimized for topical administration. It has potent effects in models of lung inflammation if administered as a dry powder inhalation. It has also demonstrated its anti-inflammatory property in a mouse model of cutaneous inflammation after topical administration. The aim of this study was to evaluate whether AWD 12-281 may be capable of penetrating human skin. Therefore a new guinea-pig model of allergic skin inflammation had to be developed. In ovalbumin-sensitized guinea-pigs, intracutaneous administration of ovalbumin results in a rapid development of allergic skin wheals. Topically administered AWD 12-281 was capable of reducing the development of wheals, indicating that this compound can penetrate the stratum corneum of guinea-pig skin as a predictor of human skin penetration. A secondary aim was the evaluation of a T cell subtype preference of AWD 12-281 since PDE4 inhibitors are said to preferentially inhibit Th2-type cytokines. Therefore, the effects of AWD 12-281 on a broad spectrum of Th1- and Th2-type cytokines were studied in tissue homogenates after allergen challenge in sensitized mice and in supernatants of anti CD3/anti-CD28-stimulated peripheral blood mononuclear cells (PBMCs). In both models, AWD 12-281 suppressed both T cell subtype cytokines indicating a broad spectrum activity of AWD 12-281. A further issue was to determine the duration of action and the concentration-response relationship of the topical activity of AWD 12-281 using a model of acute local inflammation--the arachidonic-acid-induced mouse ear oedema. The compound exhibited a dose-dependent effect with a minimally effective concentration of 0.3%; after repeated administration the minimally effective concentration was found to be 0.03%. A single administration of a 3% solution resulted in significant suppression of inflammation even 48 h after treatment. In conclusion, our results indicate that AWD 12-281 is a very promising drug candidate not only for the treatment of lung inflammation using inhalative administration but also for the treatment of atopic dermatitis.     

UV-induced erythema model: a tool in dermatopharmacology for testing the topical activity of non-steroidal anti-inflammatory agents in man

UV-induced erythema is a well known inflammatory model applied both in animal and human skin to test the activity of topical non-steroidal anti-inflammatory compounds in a great variety of pharmaceutical formulations. The aim of this study was to evaluate the inhibitory efficacy of piroxicam in two different topical formulations (cream 0.5, 1 and 1.5% and gel 1%) as compared to three non-steroidal compounds, benzydamine, etofenamate and indomethacin (cream 5%), on erythema induced after UV-injury on the back of 5 healthy subjects. The results showed that piroxicam in cream formulation, indomethacin cream and etofenamate gel have a similar effect, decreasing the erythema size 7 h after irradiation. However, benzydamine cream and piroxicam gel showed no effect with this method. We may conclude that this model is adequate and precise for selecting the most appropriate galenic dosage form for an active compound in terms of its clinical efficacy when topically administered.     

The role of PKC/ERK1/2 signaling in the anti-inflammatory effect of tetracyclic triterpene euphol on TPA-induced skin inflammation in mice

Inflammation underlies the development and progression of a number of skin disorders including psoriasis, atopic dermatitis and cancer. Therefore, novel antiinflammatory agents are of great clinical interest for prevention and treatment of these conditions. Herein, we demonstrated the underlying molecular mechanisms of the antiinflammatory activity of euphol, a tetracyclic triterpene isolated from the sap of Euphorbia tirucalli, in skin inflammation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in mice. Topical application of euphol (100 μg/ear) significantly inhibited TPA-induced ear edema and leukocyte influx through the reduction of keratinocyte-derived chemokine (CXCL1/KC) and macrophage inflammatory protein (MIP)-2 levels. At the intracellular level, euphol reduced TPA-induced extracellular signal-regulated protein kinase (ERK) activation and cyclooxygenase-2 (COX-2) upregulation. These effects were associated with euphol's ability to prevent TPA-induced protein kinase C (PKC) activation, namely PKCα and PKCδ isozymes. Our data indicate that topical application of euphol markedly inhibits the inflammatory response induced by TPA. Thus, euphol represents a promising agent for the management of skin diseases with an inflammatory component.     

Photocarcinogenesis study of aloe vera [CAS NO. 481-72-1(Aloe-emodin)] in SKH-1 mice (simulated solar light and topical application study)

The popular recognition of the Aloe barbadensis Miller (Aloe vera) plant as a therapeutic dermatologic agent has led to the widespread incorporation of Aloe vera leaf extracts in skincare products. Studies have suggested that Aloe vera in skincare preparations may enhance the induction of skin cancer by ultraviolet radiation. A 1-year study was conducted in mice to determine whether the topical application of creams containing Aloe vera plant extracts (aloe gel, whole leaf, or decolorized whole leaf) or creams containing aloe-emodin would enhance the photocarcinogenicity of simulated solar light (SSL). 1-YEAR STUDY: groups of 36 male and 36 female Crl:SKH-1 (hr -/hr -) hairless mice received topical applications of control cream or creams containing 3% or 6% (w/w) aloe gel, whole leaf, or decolorized whole leaf or 7.46 or 74.6 μg/g aloe-emodin to the dorsal skin region each weekday morning. The mice were irradiated with SSL emitted from filtered 6 kW xenon arc lamps each weekday afternoon. The topical applications of creams and irradiance exposures were conducted 5 days per week for a period of 40 weeks. A 12-week recovery/observation period followed the 40-week treatment/exposure period. Additional groups of 36 male and 36 female mice received no cream and were exposed to 0.00, 6.85, 13.70, or 20.55 mJ?CIE/cm2 SSL per day. Mice that received no cream treatment and were exposed to increasing levels of SSL showed significant SSL exposure-dependent decreases in survival and significant increases in the in-life observations of skin lesion onset, incidence, and multiplicity, and significant SSL exposure-dependent increases in the incidences and multiplicities of histopathology-determined squamous cell nonneoplastic skin lesions (squamous hyperplasia and focal atypical hyperplasia) and squamous cell neoplasms (papilloma, carcinoma in situ, and/or carcinoma). Squamous cell neoplasms were not detected in mice that received no SSL exposure. The topical treatment with the control cream of mice that were exposed to SSL did not impart a measurable effect when compared with comparable measurements in mice that received no cream treatment and were exposed to the same level of SSL, suggesting that the control cream used in these studies did not alter the efficiency of the SSL delivered to mice or the tolerability of mice to SSL. The application of aloe gel creams to mice had no effect on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity. The administration of aloe gel creams to male mice had no effect on the incidences or multiplicities of histopathology-determined squamous cell nonneoplastic skin lesions or neoplasms. Female mice treated with aloe gel creams (3% and 6%) had significantly increased multiplicities of squamous cell neoplasms. There were no treatment-related effects on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity in mice treated with the whole leaf creams. In male mice exposed to SSL and treated with the 6% whole leaf cream, a significant increase was observed in the multiplicity of squamous cell neoplasms. Female mice exposed to SSL and treated with the 3% whole leaf creams had significantly decreased multiplicity of squamous cell nonneoplastic lesions and significantly increased multiplicity of squamous cell neoplasms. Female mice exposed to SSL and treated with the 6% whole leaf cream had significantly decreased multiplicity of squamous cell nonneoplastic lesions. The application of decolorized whole leaf creams to mice had no effect on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity. Male mice administered the 3% decolorized whole leaf cream had significantly increased multiplicity of squamous cell neoplasms. Female mice administered the 3% decolorized whole leaf cream had significantly decreased multiplicity of squamous cell nonneoplastic skin lesions and significantly increased multiplicity of squamous cell neoplasms. In female mice that received the 6% decolorized whole leaf cream, there was a significant increase in the multiplicity of squamous cell neoplasms. As with the Aloe vera plant extracts, the application of aloe-emodin creams to mice had no measurable effect on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity. The administration of aloe-emodin creams to male mice had no effect on the incidence or multiplicity of histopathology-determined nonneoplastic skin lesions or squamous cell neoplasms. Female mice treated with the 74.6 μg/g aloe-emodin cream had significantly decreased multiplicity of histopathology-determined squamous cell nonneoplastic skin lesions and significantly increased multiplicity of squamous cell neoplasms. CONCLUSIONS: these experiments investigated the potential of topical application of creams containing extracts of Aloe barbadensis Miller plant (aloe gel, whole leaf, or decolorized whole leaf) or aloe-emodin to alter the photocarcinogenic activity of filtered xenon arc simulated solar light (SSL) in male and female SKH-1 hairless mice. Data on skin lesions were collected both on digital images during the in-life phase and by histopathologic evaluation at necropsy. No effects of creams upon SSL-induced skin lesions were identified from data collected during the in-life phase. ALOE GEL OR ALOE-EMODIN: under the conditions of these studies, there was a weak enhancing effect of aloe gel or aloe-emodin on the photocarcinogenic activity of SSL in female but not in male SKH-1 mice based on an increase in the multiplicity of histopathologically-determined squamous cell neoplasms. ALOE WHOLE LEAF OR DECOLORIZED WHOLE LEAF: under the conditions of these studies, there was a weak enhancing effect of aloe whole leaf or decolorized whole leaf on the photocarcinogenic activity of SSL in both male and female SKH-1 mice based on an increase in the multiplicity of histopathologically-determined squamous cell neoplasms.     

Effect of topically applied resveratrol on cutaneous herpes simplex virus infections in hairless mice

Resveratrol (3,5,4'-trihydroxystilbene) is a natural component of certain foods, such as grapes, that has been shown to have anti-herpes simplex virus (HSV) activity in vitro. To determine if it is active in vivo, the abraded epidermis of SKH1 mice were infected with HSV-1 and topically treated with 12.5 or 25% resveratrol cream or cream only. Initial studies demonstrated that: (1). 25% resveratrol cream topically applied two, three, or five times a day effectively suppressed lesion development whereas 12.5% resveratrol cream effectively suppressed lesion formation when applied five times a day starting 1h after infection; (2). when treatment was begun 1, 6, or 12h after infection, both 12.5 and 25% resveratrol were effective at 1 and 6h after infection, but not if applied 12h after infection. Comparative studies between resveratrol cream, 10% docosanol cream (Abreva) and 5% acyclovir ointment (Zovirax) were also carried out. When treatment was begun 1h after infection and repeated every 3h five times a day for 5 days, 12.5 and 25% resveratrol significantly (P=0.0001) inhibited the development of HSV-1 induced skin lesions. Acyclovir was as effective (P=0.0001) as resveratrol. Animals that were topically treated with docosanol were not protected and developed lesions in a manner indistinguishable from cream only controls. These studies were repeated with an HSV-1 acyclovir-resistant virus. As before, 12.5 and 25% resveratrol cream effectively suppressed lesion formation. The skin of resveratrol-treated animals showed no apparent dermal toxicity such as erythema, scaling, crusting, lichenification, or excoriation. These studies demonstrate that topically applied resveratrol inhibits HSV lesion formation in the skin of mice.