{"title":"Immunopotentiating effect of Khamira Marwarid, an herbo-mineral preparation.","authors":"Farah Khan, S Ali, B A Ganie, I Rubab","doi":"10.1358/mf.2009.31.8.1419719","DOIUrl":null,"url":null,"abstract":"<p><p>This study investigated the immunopotentiating effect of Khamira Marwarid (KM), an herbo-mineral Unani preparation, in an animal model. KM was administered to mice orally at a dose level of 2 g/kg body weight for 5, 10, 15 or 30 days, following which the animals were sacrificed for hematology and immune function testing, including lymphoid organ weight and cellularity. The group of animals receiving KM showed a significant increase (P < 0.05) in the relative organ (spleen and thymus) weight. Cellularity of the spleen and bone marrow also increased significantly (P < 0.01). Groups receiving KM for 10 and 15 days showed an increase in hemoglobin, red blood cells (RBCs) and total white blood cells (WBCs) (P < 0.01). The humoral immune response, evaluated by the plaque-forming cell (PFC) assay after challenging the mice with goat RBCs, was better in all treated groups when compared to controls. Maximum hemagglutination titer was obtained in mice treated with KM for 15 days. Ovalbumin-specific serum IgG levels in the treated mice also increased significantly (P < 0.01), suggesting an immunopotentiating effect for the preparation. Administration of KM resulted in elevated levels of IgG2a and IgG2b. A comparison of anti-ovalbumin IgE and IgG was also done; anti-ovalbumin IgE decreased, with a concomitant increase in anti-ovalbumin IgG. Administration of KM for 10 or 15 days elicited an increase in the delayed-type hypersensitivity (DTH) response. Taken together, the results suggest an immunostimulatory effect for KM through a mechanism leading to a Th1-dominant immune state.</p>","PeriodicalId":18443,"journal":{"name":"Methods and findings in experimental and clinical pharmacology","volume":"31 8","pages":"513-22"},"PeriodicalIF":0.0000,"publicationDate":"2009-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"18","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Methods and findings in experimental and clinical pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1358/mf.2009.31.8.1419719","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 18
Abstract
This study investigated the immunopotentiating effect of Khamira Marwarid (KM), an herbo-mineral Unani preparation, in an animal model. KM was administered to mice orally at a dose level of 2 g/kg body weight for 5, 10, 15 or 30 days, following which the animals were sacrificed for hematology and immune function testing, including lymphoid organ weight and cellularity. The group of animals receiving KM showed a significant increase (P < 0.05) in the relative organ (spleen and thymus) weight. Cellularity of the spleen and bone marrow also increased significantly (P < 0.01). Groups receiving KM for 10 and 15 days showed an increase in hemoglobin, red blood cells (RBCs) and total white blood cells (WBCs) (P < 0.01). The humoral immune response, evaluated by the plaque-forming cell (PFC) assay after challenging the mice with goat RBCs, was better in all treated groups when compared to controls. Maximum hemagglutination titer was obtained in mice treated with KM for 15 days. Ovalbumin-specific serum IgG levels in the treated mice also increased significantly (P < 0.01), suggesting an immunopotentiating effect for the preparation. Administration of KM resulted in elevated levels of IgG2a and IgG2b. A comparison of anti-ovalbumin IgE and IgG was also done; anti-ovalbumin IgE decreased, with a concomitant increase in anti-ovalbumin IgG. Administration of KM for 10 or 15 days elicited an increase in the delayed-type hypersensitivity (DTH) response. Taken together, the results suggest an immunostimulatory effect for KM through a mechanism leading to a Th1-dominant immune state.