title: Cardiospermum halicacabum inhibits cyclophosphamide induced immunosupression and oxidative stress in mice and also regulates iNOS and COX-2 gene expression in LPS stimulated macrophages.
abstract: The effect of a methanolic extract of Cardiospermum halicacabum L was studied against cyclophosphamide (CTX)-induced toxicity in mice. Administration of CTX (25 mg/kg b.wt, i.p.) for 10 days produced significant myelosuppression as evidenced by a decreased WBC count and bone marrow cellularity. Co-treatment with Cardiospermum significantly increased the total WBC count, bone marrow cellularity and α-esterase positive cells, and the relative organ weights of spleen as well as thymus compared to the CTX alone treated group. Cardiospermum further reduced the enhanced levels of ALP, GPT, LPO, and proinflammatory cytokine TNF-α, and also significantly increased the glutathione (GSH) level in CTX treated animals. The lowered levels of other cytokines like IFN-γ, IL-2, GM-CSF, after CTX treatment were also found to be increased by extract administration. Histopathological analysis of small intestine also suggested reduction of CTX-induced intestinal damage. Moreover the extract down-regulated the inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) mRNA expression in LPS stimulated macrophages. These studies indicate that C. halicacabum could reduce cyclophosphamide induced oxidative stress and immunosupression through enhancing the antioxidant status and immunomodulation by stem cell proliferation.
authors.affiliation: Amala Cancer Research Centre, Amala Nagar, Kerala State, India.
authors.forename: P
authors.initials: P
authors.lastname: Pratheeshkumar
authors.forename: Girija
authors.initials: G
authors.lastname: Kuttan
mesh_terms: D000818:Animals; D018906:Antineoplastic Agents, Alkylating / Q000494:pharmacology; D001853:Bone Marrow / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000235:genetics*; D003520:Cyclophosphamide / Q000494:pharmacology*; D016207:Cytokines / Q000187:drug effects; D015870:Gene Expression; D005786:Gene Expression Regulation / Q000187:drug effects; D005978:Glutathione / Q000032:analysis; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000276:immunology; D008264:Macrophages / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D052247:Nitric Oxide Synthase Type II / Q000235:genetics*; D018384:Oxidative Stress / Q000187:drug effects*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis / Q000187:drug effects; D029631:Sapindaceae / Q000737:chemistry*; D013154:Spleen / Q000502:physiology; D013950:Thymus Gland / Q000502:physiology
chemical_list: D018906:Antineoplastic Agents, Alkylating; D016207:Cytokines; D008070:Lipopolysaccharides; D010936:Plant Extracts; D012333:RNA, Messenger; D003520:Cyclophosphamide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D005978:Glutathione