CN109453362A - 一种保护胃黏膜及抗幽门螺旋杆菌的组合物及其应用 - Google Patents
一种保护胃黏膜及抗幽门螺旋杆菌的组合物及其应用 Download PDFInfo
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Abstract
本发明属于保健食品技术领域,尤其涉及一种保护胃黏膜及抗幽门螺旋杆菌的组合物及其应用。本发明提供了一种组合物,所述组合物的原料包括:猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽。本发明采用猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽这四种天然药食两用植物提取物进行组合使用,实验结果表明,本发明组合物对胃粘膜损伤具有显著的保护作用,对小鼠幽门螺旋杆菌感染者和人幽门螺旋杆菌感染者均具有显著的清除作用,并且,本发明组合物由四种天然药食两用植物提取物组成,适合长期使用、不良反应少。
Description
技术领域
本发明属于保健食品技术领域,尤其涉及一种保护胃黏膜及抗幽门螺旋杆菌的组合物及其应用。
背景技术
胃粘膜是胃的保护伞,胃粘膜保护机制是指长期暴露于腔内pH、渗透压和温度的广泛变化而不受损伤,并能对抗细菌产物及其引起的炎症反应。当机体受到幽门螺旋杆菌感染、服用非甾体消炎药、胃酸过多,以及应激、心理因素、吸烟、酗酒等因素破坏了胃粘膜的保护机制时,将会导致胃粘膜的损伤,从而出现胃溃疡、胃炎等胃部疾病及不适症状,中医属“胃脘痛”、“胃气痛”、“吞酸”等范畴。
2017年《第五次全国幽门螺旋杆菌感染处理共识》报告中指出,目前我国幽门螺旋杆菌(H.pylori)感染率仍达到50%,幽门螺旋杆菌作为一种革兰氏阴性微量需氧、弯曲性杆状细菌,它会产生大量的尿素酶,在胃中生成氨,从而改变胃的生理条件,造成胃泌素和生长抑制的分泌紊乱;它会使胃黏膜的疏水性下降;它还会直接破坏上皮细胞释放炎性介质,形成氧自由基等,引发胃黏膜局部炎症反应,使胃酸分泌过多,破坏正常的胃黏膜屏障,从而诱发胃十二指肠溃疡,而由幽门螺旋杆菌感染导致的胃粘膜防御机制减弱是引起胃溃疡难以治疗的重要因素。
目前针对幽门螺旋杆菌感染,主要采用抗生素、抗酸、抑酸药物进行治疗,抗生素疗法具有较强的副作用,并且,由于H.pylori耐药菌株的出现,不良事件的发生以及依从性的下降等原因,抗生素疗法的有效性不断下降,在一些研究报道中,抗生素疗法的有效率已不足70%。并且,现有疗法对幽门螺旋杆菌导致的胃粘膜受损治疗具有对机体损伤较大、容易复发。
发明内容
有鉴于此,本发明提供了一种保护胃黏膜及抗幽门螺旋杆菌的组合物及其应用,用于解决现有疗法对幽门螺旋杆菌导致的胃粘膜受损治疗具有较强的副作用、容易复发的问题。
本发明的具体技术方案如下:
一种组合物,所述组合物的原料包括:猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽。
猴头菇(Hericium erinaceus)又名猴头、猴头蘑、猴头菌、刺猬菌等,是一种大型真菌,属担子菌纲、多孔菌目、齿菌科、猴头属,因其子实体形状像猴子头部而得名。猴头菇包括丰富的蛋白质、脂肪、纤维素、多糖,还含有16种氨基酸,其中有8种人体必需氨基酸,且各种氨基酸的比例与人体需要接近。猴头菌的药效成分主要有多糖、低聚糖、甾醇、脂肪酸、猴头菌素、猴头酮等,而近年来的药理和临床研究表明,猴头菌具有助消化、利五脏的功能,对慢性胃炎、十二指肠溃疡、胃溃疡等多种消化道疾病均有较好的疗效。
西兰花种子提取物是由十字花科西兰花(Brassica oleracea var.italicaPlenck)的种子提取得到。十字花科蔬菜(包括西兰花、抱子甘蓝、卷心菜、空心菜、芥蓝菜、芥菜、白菜等)均富含硫代葡萄糖酸盐(Glucosinolates,GLS,简称硫苷),萝卜硫苷(Glucoraphanin,4甲基硫氧丁基硫苷)作为硫苷中的其中一种,在经黑芥子硫苷酸酶水解后形成活性物质,主要包括异硫氰酸盐(如莱菔硫烷、苯乙基异硫氰酸盐)及吲哚(如吲哚-3-甲醇),其中莱菔硫烷(sulforaphane,SFN,又称莱菔子素,萝卜硫素)是异硫氰酸盐的主要特征性成分,是一种具有较强抗癌作用的植物化学活性物质。目前报道对于人膀胱癌、前列腺癌、骨肉瘤、脑胶质瘤、成神经管细胞瘤、乳腺癌、结肠癌、胰腺癌、肝癌、皮肤癌及白血病等多个肿瘤细胞系均有一定的抑瘤作用。
姜黄(Curcuma longa Linn)来源于植物姜黄的干燥根茎,其最早记载于《新修本草》:“叶根都似郁金,花春生于根,与苗并出,夏花烂,无子,根有黄、青、白三色。其作之方法与郁金同尔。”姜黄味苦、辛、性温,归脾、经,具有破血行气、通经止痛之功效,可用于血瘀气滞诸证,胸腹肋痛,妇女痛经,闭经,风湿痹痛等多种病症。姜黄素可影响胃酸、胆汁、胰液等的分泌与排泄,具有明显的抗溃疡作用。近些年来,有关姜黄护胃、保肝、降血脂、抗氧化、增强免疫力等多方面保健功效已经成为学术研究热点。
小麦低聚肽是以小麦谷阮粉为原料,经过酶解、提纯等步骤加工制得,具有较高的含量和均衡的氨基酸组成。同时小麦低聚肽粉还具有水溶性好、稳定性强、易于消化吸收、蛋白含量高等优势,因此可作为谷氨酰胺(Gln)补充剂的优良选择。小麦低聚肽中Gln的含量为(23.54±0.49%)远高于其他食源性低聚肽类产品,谷氨酰胺对胃肠黏膜的生长与健康有着重要的积极作用,谷氨酰胺能促进内源性前列腺素的合成、抑制炎性细胞因子分泌,减轻炎症损伤、增强胃黏膜抗氧自由基损伤的能力、增强胃黏膜黏液层屏障功能、抑制细胞凋亡、调节免疫应答、参与消化道黏膜细胞修复。
优选的,所述猴头菇提取物、所述西兰花种子提取物、所述姜黄提取物和所述小麦低聚肽的质量比为(5~9):(0.5~2):(1~3):(1~3)。
优选的,所述猴头菇提取物、所述西兰花种子提取物、所述姜黄提取物和所述小麦低聚肽的质量比为(7~9):(0.5~2):(1~3):(1~3)。
优选的,所述猴头菇提取物、所述西兰花种子提取物、所述姜黄提取物和所述小麦低聚肽的质量比为8:1:2:2。
优选的,所述西兰花种子提取物为西兰花种子水提物。
西兰花种子水提物是由十字花科西兰花的种子经热水提取、固液分离、浓缩、喷雾干燥等步骤制成。
本发明中,猴头菇提取物为猴头菇子实体经过提取得到的猴头菇多糖;西兰花种子水提物由十字花科蔬菜西兰花经水提取、分离、浓缩、干燥得到;姜黄提取物由姜黄通过溶剂提取得到,优选由姜黄通过溶剂提取再经大孔树脂分离得到;小麦低聚肽由谷朊粉经酶解、提纯得到。
本发明中,猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽为粉末。
本发明还提供了上述技术方案所述组合物在制备保护胃黏膜及抗幽门螺旋杆菌的保健品或食品中的应用。
本发明还提供了一种食品,包括上述技术方案所述的组合物。
本发明还提供了一种保健品,包括上述技术方案所述的组合物和食品上可接受的辅料。
优选的,所述食品上可接受的辅料包括矫味剂、填充剂、包衣材料、润滑剂和崩解剂中的一种或多种。
优选的,所述保健品的剂型选自片剂、粉剂或硬胶囊。
本发明中,粉剂可通过以下步骤制备得到:将猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽混合,加入麦芽糊精、安赛蜜、果汁粉、和二氧化硅后,置于三维混合机中,混合30min,出料,得到粉料,采用3层PE袋密封保存;采用颗粒机,选用80mm铝箔膜进行粉料的袋包包装,袋包过程中检查、保证袋包装量稳定性、袋包密封性;检验合格后,包装,按照企业标准检验,检验合格后入库。
本发明中,片剂可通过以下步骤制备得到:将猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽混合,再加入微晶纤维素、磷酸氢钙、羧甲淀粉钠和二氧化硅混合25min,加入硬脂酸镁混合5min后出料备用,得到粉料,采用18*9mm椭圆形模具进行粉料压片,压片过程中控制重量差异、崩解时限和素片硬度,再加入深黄色薄膜包衣粉进行包衣,检验合格后,进行包装,最后按照企业标准检验,检验合格后入库。
综上所述,本发明提供了一种组合物,所述组合物的原料包括:猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽。本发明采用猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽这四种天然药食两用植物提取物进行组合使用,实验结果表明,猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽具有协同作用,使得本发明组合物对胃粘膜损伤具有显著的保护作用,对小鼠幽门螺旋杆菌感染者和人幽门螺旋杆菌感染者均具有显著的清除作用,并且,本发明组合物由四种天然药食两用植物提取物组成,适合长期使用、不良反应少。
具体实施方式
本发明提供了一种保护胃黏膜及抗幽门螺旋杆菌的组合物及其应用,用于解决现有疗法对幽门螺旋杆菌导致的胃粘膜受损治疗具有较强的副作用、容易复发的问题。
下面将对本发明实施例中的技术方案进行清楚、完整地描述,显然,所描述的实施例仅仅是本发明一部分实施例,而不是全部的实施例。基于本发明中的实施例,本领域普通技术人员在没有做出创造性劳动前提下所获得的所有其他实施例,都属于本发明保护的范围。
实施例1
本实施例提供了不同组别的供试品,以重量份计,供试品的原料如表1所示。
表1不同组别的供试品
实施例2
本实施例对实施例1供试品进行胃粘膜保护作用的检测。
(1)实验动物
选用SD或Wistar健康大鼠,单一性别,180g~220g,每组8~12只。
(2)仪器与试剂
无水乙醇、甲醛、石蜡、环保透明剂、95%乙醇、曙红、苏木素、解剖器械、游标卡尺、酒精或醋酸、病理制片系统、生物显微镜。
(3)实验方案
将大鼠随机分为13组,包括单剂量实验组1~4、实验组1~7、正常对照组和模型组。单剂量实验组1~4、实验组1~7分别灌胃给予136.5mg/kg.bw的供试品(供试品采用纯净水进行溶解),1次/天,连续30天,正常对照组和模型对照组采用相同方法给予同体积纯净水。各组大鼠灌胃30天后,全部大鼠严格禁食24小时(不禁水),此期间亦禁止给予供试品液或纯净水。除正常对照组外,所有实验组大鼠给予无水乙醇1.0mL/只,1小时后处死动物,暴露完整胃,结扎幽门,灌注适量10%甲醛溶液,固定20min,然后沿胃大弯剪开,洗净胃内容物,展开胃粘膜,在体视解剖显微镜下或肉眼下用游标卡尺测量出血点或出血带的长度和宽度。采用表2进行急性酒精损伤肉眼观察评分,因宽度所代表损伤的严重性远较长度大,故双倍积分。并进行胃粘膜损伤程度的检测和病理组织学观察及评分。
胃粘膜损伤程度以损伤发生率(%)、损伤积分指数和损伤抑制率表示。损伤发生率(%)=某组出现出血或溃疡的大鼠数量/该组大鼠数量×100%;损伤积分指数=组病变总积分总和/组动物数量;损伤抑制率(%)=(A-B)/A*100%(A、B分别为模型对照组与实验组的组损伤总积分总和)。
病理组织学观察及评分:大体检查完毕,将每只大鼠胃粘膜损伤最严重的部位切下,固定于10%甲醛溶液,常规制片,HE染色,镜下观察。注意选择胃粘膜正横切面,包括粘膜全层的区域观察。评分方法:以充血、出血、粘膜细胞变性坏死在整个粘膜上皮层的累及程度分为5级。充血权重为1,出血权重为2,上皮细胞变性坏死权重为3,评分标准及病变总积分公式见表3。
表2急性酒精损伤显微镜或肉眼观察评分标准
表3急性胃粘膜损伤镜下评分标准
(4)实验结果
1)临床观察结果
实验期间,对各组大鼠进行临床观察,各组大鼠体型、被毛、皮肤、粪便、肌肉张力、步态、精神、呼吸等均未见异常,体重、摄食量均无统计学差异,其中体重数据请见表4。
表4各组大鼠体重数据
2)各组大鼠胃粘膜损伤结果
请参阅表5,为各组大鼠胃粘膜损伤结果。结果表明,与正常对照组相比,模型对照组大鼠胃粘膜损伤积分指数明显升高,具有统计学差异(P<0.01),损伤发生率为100%;与模型对照组比较,单剂量实验组1、4(P<0.05)与实验组1~4大鼠胃粘膜损伤积分指数显著下降(P<0.05),实验组5~7大鼠胃粘膜损伤积分明显指数下降(P<0.01);与单剂量实验组1~4相比,实验组1~4无显著差异(P>0.05),实验组5、6具有显著差异(P<0.05),实验组7具有极显著差异(P<0.01)。与实验组5、6相比,实验组7大鼠胃粘膜损伤积分指数显著下降(P<0.05)。以上结果显示实验组7大鼠胃粘膜损伤积分指数最低、损伤发生率最低、损伤抑制率最高,实验组7供试品能够使大鼠胃粘膜损伤评分显著降低,优于其它实验组,并具有极显著差异。
表5各组大鼠胃粘膜损伤结果
组别 | 动物数(只) | 损伤总积分 | 损伤发生率(%) | 损伤抑制率(%) |
正常对照组 | 10 | 0±0.00 | 0 | - |
模型组 | 10 | 16.38±1.41<sup>△△</sup> | 100 | - |
单剂量实验组1 | 10 | 11.85±1.14* | 80 | 27.66 |
单剂量实验组2 | 10 | 15.4±0.97 | 90 | 5.96 |
单剂量实验组3 | 10 | 16.09±0.65 | 90 | 1.77 |
单剂量实验组4 | 10 | 11.14±0.27* | 80 | 32.00 |
实验组1 | 10 | 10.68±1.07* | 80 | 37.88 |
实验组2 | 10 | 10.54±0.598* | 70 | 37.15 |
实验组3 | 10 | 10.54±0.73* | 70 | 36.96 |
实验组4 | 10 | 10.95±0.57* | 70 | 32.63 |
实验组5 | 10 | 8.27±0.63**<sup>#</sup> | 70 | 38.92 |
实验组6 | 10 | 8.09±0.32**<sup>#</sup> | 60 | 42.37 |
实验组7 | 10 | 6.08±0.71**<sup>##</sup> | 50 | 51.72 |
与正常对照组比较,△P<0.05,△△P<0.01;与模型组比较,*P<0.05,**P<0.01;与单剂量实验组比较,#P<0.05,##P<0.01。
3)病理组织学观察结果
请参阅表6,为各组大鼠病理学观察结果。结果表明,模型对照组大鼠胃粘膜充血,局部粘膜出血、上皮细胞坏死脱落,粘膜下层水肿、炎细胞浸润,部分大鼠可见粘膜下层出血,而实验组1~7均可见以上症状不同程度的减轻,实验结果见表6。结果显示,与正常对照组比较,模型对照组大鼠病理组织学评分升高,具有统计学差异(P<0.01);与模型对照组比较,单剂量实验组1、4和实验组1~4均能够降低大鼠病理学组织学评分(P<0.05),实验组5~7能够显著降低大鼠病理学组织学评分(P<0.01);与单剂量实验组1~4相比,实验组5、6能够降低大鼠病理学组织学评分(P<0.05),实验组7能够使大鼠病理学组织评分极显著降低(P<0.01)。结果表明实验组7大鼠病理组织学评分最低,实验组7供试品能够使大鼠胃粘膜损伤评分显著降低,优于其它实验组,并具有极显著差异。
表6各组大鼠病理组织学观察结果
与正常对照组比较,△P<0.05,△△P<0.01;与模型组比较,*P<0.05,**P<0.01;与单剂量实验组比较,#P<0.05,##P<0.01。
实施例3
本实施例对实施例1供试品进行抗体内幽门螺旋杆菌作用的检测。
(1)实验动物
幽门螺旋杆菌(H.pylori)感染BALB/c小鼠130只,正常BALB/c小鼠10只,6~8周龄,重17~20g,雌雄各半。每只小鼠每日折合以上大鼠剂量灌胃1次。
(2)仪器与试剂
快速尿素酶试纸、无水乙醇、甲醛、石蜡、环保透明剂、95%乙醇、曙红、苏木素、解剖器械、游标卡尺、酒精或醋酸、病理制片系统、生物显微镜。
(3)实验方案
首先将130只BALB/c小鼠以三联疗法清除胃内杂菌,雌雄均各半。病理模型组(130只):将H.pylori菌株以0.4ml/次(1×109CFU/mL)×5次,感染1周。灌胃前先禁食禁水12小时,灌胃后禁食禁水2小时,末次灌胃后4w随机抽取10只剖杀,剖杀前禁食禁水24小时。剖杀后,观察小鼠胃粘膜大体标本形态学,并作H.Pytori培养、快速尿素酶实验检测造模是否成功。
将成功造模的小鼠120只随机分成12组进行体内治疗实验,治疗实验分成模型对照组和单剂量实验组1~4、实验组1~7。单剂量实验组1~4、实验组1~7供试品液灌胃30天,灌胃剂量201.5g/kg.bw,末次灌胃后1天将10只剖杀,剖杀前禁食禁水24小时。模型对照组(10只)不给任何治疗。
正常BALB/c小鼠10只作为正常对照组给予同等浓度的麦芽糊精灌胃,与上述组别同期抽取10只剖杀,剖杀前禁食禁水24小时。
剖杀后的小鼠使用细菌学进行H.pylori培养、快速尿素酶实验来检测H.pylori。
H.pylori培养:大鼠胃黏膜活检标本,分别取自大鼠胃窦部,将大鼠胃黏膜组织放入20%葡萄糖(GS)运送液中,于4℃3h内送至实验室,将其中部分标本的组织黏膜研成匀浆,涂布于H.pylori专用培养基,在微需氧环境中37℃培养3~6d,3d后逐日观察菌落生长情况。对可疑菌落作涂片染色、镜检。如具有典型的菌落特征、菌体形态和染色性,且快速尿素酶实验阳性者鉴定为H.pylori。快速尿素酶实验:取新鲜组织标本一小粒按试剂盒说明书进行快速尿素酶实验。结果请参阅表7,结果显示,与正常对照组比较,模型组小鼠通过细菌学检查以及尿素酶检测,均检出幽门螺旋杆菌100%,证明建模成功。结果显示,模型组小鼠胃内的H.pylori均未被清除,根除率为0%。无H.pylori感染的正常对照组中,10只小鼠均未发现H.pylori生长。单剂量实验组1~4和实验组1~4与模型对照组相比,具有一定的幽门螺旋杆菌清除率;实验组5、6对幽门螺旋杆菌的根除率为60%~70%,实验组7对幽门螺旋杆菌的根除率为40%~50%。结果表明实验组7对幽门螺旋杆菌的根除率最高,明显优于其它实验组。
表7各组小鼠H.pylori检出情况
组别 | 动物数 | 细菌学检查阳性率/% | 尿素酶阳性率/% |
正常对照组 | 10 | 0 | 0 |
模型组 | 10 | 100 | 100 |
单剂量实验组1 | 10 | 80 | 90 |
单剂量实验组2 | 10 | 70 | 60 |
单剂量实验组3 | 10 | 70 | 70 |
单剂量实验组4 | 10 | 90 | 100 |
实验组1 | 10 | 70 | 60 |
实验组2 | 10 | 70 | 70 |
实验组3 | 10 | 70 | 70 |
实验组4 | 10 | 70 | 70 |
实验组5 | 10 | 70 | 60 |
实验组6 | 10 | 60 | 60 |
实验组7 | 10 | 40 | 40 |
实施例4
本实施例对实施例1供试品进行人体内幽门螺旋杆菌抑制实验。
(1)研究对象
经胃幽门螺旋杆菌吹气C13检测呈阳性者,年龄18-65岁。
研究对象排除标准:妊娠、哺乳期妇女;短期内服用具有治疗胃部不适的食品或药品、近4周使用质子泵抑制剂、抗生素、H2受体拮抗剂、铁制剂及进行过H.pylori根除史者;患有上消化道出血、穿孔及其他严重消化道疾病者。
符合以上条件的受试者共纳入幽门螺旋杆菌C13检测阳性者84人,并记录初始C13检测值。
(2)实验方案
将以上研究对象随机分为单剂量实验组1~4、实验组1~7和空白对照组,按照以上分组给予以上供试品,每日1次,每次1300mg/60kg,空腹服用。服用时将以上受试物加入100mL温水,冲调搅匀后即可饮用。疗程共30天,试食30天后,停药4周,C13呼气实验判断阴性者为H.pylori根除,计算根除率、转阴率。
试食过程中,同时记录不良反应评价,依照表8人体试食实验症状轻重分级评分。
评价指标:1、DOB值(C13吹气检验的指标)<4即为转阴,临床上DOB值不能够降到4以下认为治疗失败;2、主观胃部症状观察,人体试食实验症状轻重分级请见表8。
表8人体试食实验症状轻重分级
(3)实验结果
1)请参阅表9,为试食前后C13检验结果。C13吹气检验结果显示,单剂量实验组3和实验组2都有个别转阴现象,而实验组1~6则具有一定的幽门螺旋杆菌转阴率,但实验组7的转阴率高达57.14%。结果证明,实验组7供试品清除人体内幽门螺旋杆菌的效果最强,且具有极显著差异。
表9试食前后C13检验结果
2)请参阅表10,为试食前后症状轻重观察结果。人体试食实验症状观察结果显示,试食后,与空白对照组比较,其它各组症状均有不同程度的下降。其中,与空白对照组相比,单剂量实验组1、3、4症状下降(P<0.05),实验组1~7症状显著下降(P<0.01)。与单剂量实验组1~4相比,实验组1~4症状下降(P<0.05),实验组5~7症状下降极显著(P<0.01);实验组7症状与实验组5、6相比,症状积分明显下降(P<0.05)。并且,实验组7供试品能够使得试食后总积分并且低于其它实验组,并具有极显著差异,表明实验组7具有显著的改善胃部不适症状的功能。
表10试食前后症状轻重观察结果
组别 | 纳入人数(人) | 干预后症状积分 |
空白对照组 | 7 | 12.73±0.96 |
单剂量实验组1 | 7 | 8.63±0.96* |
单剂量实验组2 | 7 | 11.75±0.96 |
单剂量实验组3 | 7 | 9.33±0.5* |
单剂量实验组4 | 7 | 9.5±0.58* |
实验组1 | 7 | 7.63±0.82**<sup>#</sup> |
实验组2 | 7 | 7.46±0.82**<sup>#</sup> |
实验组3 | 7 | 6.56±0.58**<sup>#</sup> |
实验组4 | 7 | 6.53±0.82**<sup>#</sup> |
实验组5 | 7 | 4.75±0.5**<sup>##</sup> |
实验组6 | 7 | 4.55±0.58**<sup>##</sup> |
实验组7 | 7 | 3.3±0.82**<sup>##△</sup> |
与空白对照组比较,*P<0.05,**P<0.01;实验组1~7与单剂量实验组1~4比较,#P<0.05,##P<0.01;实验组7与实验组5、6比较△P<0.05,△△P<0.01。
以上所述仅是本发明的优选实施方式,应当指出,对于本技术领域的普通技术人员来说,在不脱离本发明原理的前提下,还可以做出若干改进和润饰,这些改进和润饰也应视为本发明的保护范围。
Claims (10)
1.一种组合物,其特征在于,所述组合物的原料包括:猴头菇提取物、西兰花种子提取物、姜黄提取物和小麦低聚肽。
2.根据权利要求1所述的组合物,其特征在于,所述猴头菇提取物、所述西兰花种子提取物、所述姜黄提取物和所述小麦低聚肽的质量比为(5~9):(0.5~2):(1~3):(1~3)。
3.根据权利要求2所述的组合物,其特征在于,所述猴头菇提取物、所述西兰花种子提取物、所述姜黄提取物和所述小麦低聚肽的质量比为(7~9):(0.5~2):(1~3):(1~3)。
4.根据权利要求3所述的组合物,其特征在于,所述猴头菇提取物、所述西兰花种子提取物、所述姜黄提取物和所述小麦低聚肽的质量比为8:1:2:2。
5.根据权利要求1所述的组合物,其特征在于,所述西兰花种子提取物为西兰花种子水提物。
6.权利要求1至5任意一项所述组合物在制备保护胃黏膜和/或抗幽门螺旋杆菌的保健品或食品中的应用。
7.一种食品,其特征在于,包括权利要求1至5任意一项所述的组合物。
8.一种保健品,其特征在于,包括权利要求1至5任意一项所述的组合物和食品上可接受的辅料。
9.根据权利要求8所述的保健品,其特征在于,所述食品上可接受的辅料包括矫味剂、填充剂、包衣材料、润滑剂和崩解剂中的一种或多种。
10.根据权利要求8所述的保健品,其特征在于,所述保健品的剂型选自片剂、粉剂或硬胶囊。
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CN115363210A (zh) * | 2022-07-12 | 2022-11-22 | 澳优乳业(中国)有限公司 | 一种保护胃肠粘膜、抗幽门螺杆菌及促进胃肠蠕动的组合物及其应用 |
WO2024011771A1 (zh) * | 2022-07-12 | 2024-01-18 | 澳优乳业(中国)有限公司 | 一种保护胃肠粘膜、抗幽门螺杆菌及促进胃肠蠕动的组合物及其应用 |
CN115956675A (zh) * | 2022-12-08 | 2023-04-14 | 杭州娃哈哈科技有限公司 | 一种保护胃粘膜组合物、制备方法及其应用 |
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