Use of Apigenin in preparation of drugs for prevention and treatment on chronic obstructive pulmonary diseases
A technology for chronic obstructive pulmonary disease, used in drug combinations, respiratory diseases, pharmaceutical formulations, etc., can solve problems such as slow progress in drug treatment research, different pathogenesis, and difficulty in obtaining satisfactory curative effects.
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Embodiment 1
[0015] Embodiment 1: the preparation of compound Apigenin tablet involved in the present invention:
[0016] Take 5 grams of the compound Apigenin, add 195 grams of dextrin, mix well, and make 1000 tablets with a conventional tablet machine.
Embodiment 2
[0017] Embodiment 2: the preparation of compound Apigenin capsules involved in the present invention:
[0018] Take 5 grams of the compound Apigenin, add 195 grams of starch, mix well, and make 1000 capsules.
[0019] The following pharmacodynamic experiments will further illustrate its drug activity.
[0020] Methods: SPF grade female BALB / c mice, 18-20g, were randomly divided into normal control group, model control group, positive control group (terbutaline, 10mg / kg, intragastric administration), drug treatment group (Apigenin 5, 10, 20mg / kg, intragastric administration), 10 rats in each group. The mice were placed in a 4L container and smoked every day (Jinjian brand cigarettes, tar content less than 16mg), five times a week, for four consecutive weeks, administered by intragastric administration 1 hour before the daily smoke. One hour after fumigation, anesthetize with sodium phenobarbital, perfuse the lungs with 0.6 mL of pre-cooled PBS buffer (pH 7.0), rinse 3 times, ...
experiment example 1
[0021] Experimental Example 1: Inhibitory effect of Apigenin on the production of inflammatory mediators in bronchoalveolar lavage fluid (BALF) of COPD mice (1) Inhibitory effect of Apigenin on the production of TNFα in BALF of COPD mice
[0022] The proinflammatory cytokine TNFα is an initiating factor in the pathogenesis of COPD. The level of TNFα in COPD patients is higher than that of normal people, and the cultured bronchial epithelial cells can secrete TNFα in contact with cigarette smoke. TNFα can promote neutrophil degranulation, induce mucosal cell proliferation and hypersecretion, increase the production of IL-8 in epithelial cells, increase the production of matrix metalloproteinases in macrophages, and promote airway hyperresponsiveness. The purpose of this experiment is to investigate the effect of Apigenin on the production of TNFα in the BALF of COPD mice. The results are shown in Table 1.
[0023] Table 1 The effect of Apigenin on the production of TNFα in the...
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