Cancer is a life-threatening disease and is considered to be among the leading causes of death worldwide. Chemoresistance, severe toxicity, relapse and metastasis are the major obstacles in cancer therapy. Therefore, introducing new therapeutic agents for cancer remains a priority to increase the range of effective treatments. Terpenoids, a large group of secondary metabolites, are derived from plant sources and are composed of several isoprene units. The high diversity of terpenoids has drawn attention to their potential anticancer and pharmacological activities. Some terpenoids exhibit an anticancer effect by triggering various stages of cancer progression, for example, suppressing the early stage of tumorigenesis via induction of cell cycle arrest, inhibiting cancer cell differentiation and activating apoptosis. At the late stage of cancer development, certain terpenoids are able to inhibit angiogenesis and metastasis via modulation of different intracellular signaling pathways. Significant progress in the identification of the mechanism of action and signaling pathways through which terpenoids exert their anticancer effects has been highlighted. Hence, in this review, the anticancer activities of twenty-five terpenoids are discussed in detail. In addition, this review provides insights on the current clinical trials and future directions towards the development of certain terpenoids as potential anticancer agents.

Curcumin (CUR) has been used since ancient times to treat several ailments as it possesses many pharmacological activities. This study intended to explore the mechanism underlying the protective effects of CUR in remodeling oxidative stress and apoptotic signals in cyclophosphamide (CP)-induced pulmonary injury in albino rats. CUR was administered at a dose of 300 mg/kg/day for 7 days and on the seventh day a single dose of CP (200 mg/kg) was given. Histopathological and ultrastructural examinations of CP-intoxicated rats showed complete alveolar obstruction, thickened inter-alveolar septa, enlarged blood vessels, severe inflammatory edema with pyknotic nuclei, and disappearance of cytoplasmic organelles. Significant increases in caspase-3, malondialdehyde (MDA), and protein carbonyl (PCO) and significant decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPx) were observed. In contrast, rats that received CUR showed clear and empty lumina with single row of pneumocytes, disappearance of edema, and no interstitial electron dense bodies in rats’ lung tissues. Additionally, CUR significantly reduced caspase-3, MDA, and PCO and increased SOD and GPx. In conclusion, these findings revealed the protective effects of CUR against CP-induced pulmonary injury in rats through suppressing oxidative damage and apoptosis.

Context: The possible toxic effects of monosodium glutamate (MSG) on ovarian functions have not been thoroughly evaluated in contrast to testicular functions. Few studies documented that MSG showed histological alterations. Aims: To investigate the subacute effects of oral MSG (2 g/kg) on estrogen level and numbers of ovulated oocytes and histological changes in ovary of Sprague-Dawley (SD) rats. Methods: Virgin young adult SD female rats with a regular estrous cycle were randomly assigned to either MSG-treated group or control group, and the duration of treatment was 14-16 days for oral administration MSG or vehicle (distilled water), respectively. Results: Oral MSG treatment with doses of 2 g/kg/day showed significantly (p<0.01) reduced numbers of ovulated oocytes in the oviduct, newly formed corpora lutea, large follicles in histology of ovarian sections and attenuated serum estrogen levels. Conclusions: Subacute oral administration of MSG may negatively influence the ovarian function of young female rats via reduction of ovulated oocytes and the attenuation of estrogen level.