One of the most common tumors to cause death worldwide is colon cancer. This study aims to investigate the antitumor potency of Litophyton sp. methanolic extract (LME) against DMH-induced colon cancer in adult male rats. Group (1) normal rats served as the control, group (2) normal rats were ip-injected with LME at a dose of 100 μg/kg/day, group (3) DMH-induced colon cancer animals, and group (4) colon cancer-modeled animals were treated with LME (100 μg/kg/day) for six weeks. The results revealed that injection of LME markedly regenerated the colon cancer pathophysiological disorders; this was monitored from the significant reduction in the values of serum biomarkers (CEA, CA19.9, AFP), cytokines (TNF-α and IL1β), and biochemical measurements (ALAT, ASAT, urea, creatinine, cholesterol, and triglycerides) matched significant increase of apoptotic biomarkers (CD4+); similarly, colon DNA fragmentation, MDA, and NO levels were down-regulated. In contrast, a remarkable upregulation in colon SOD, GPx, GSH, and CAT levels was noted. Moreover, the colon histopathological architecture showed obvious regenerations. Chromatography of LME resulted in the purification of two polyhydroxylated steroids (1 and 2) with potential cytotoxic activities. LME performed therapeutic potential colon tumorigenesis; therefore, LME may have a promising chemo-preventive feature against colon cancer, probably via enhancement of the apoptosis pathway, improvement of the immune response, reduction of inflammation, or/and restoration of the impaired oxidative stress.

Background: Testicular dysfunction is one of the common side effects that results from the treatment with oxaliplatin® as a chemotherapy drug, and pharmaceutical search for agents to relieve the side effects are underway. The current study explored the possible ameliorative and regenerative effects of Costus ethanolic extract against testicular degeneration in male rats induced by oxaliplatin. Methods: Male Wistar albino rats weighing 150-200g were divided into four groups of 10 rats each as follows: group-1 control rats; group-2 rats treated orally with the extract at 50 mg/kg/day for six weeks; group-3 rats injected oxaliplatin intraperitoneally at 10 mg/kg/week for six successive weeks; group-4 rats were injected intraperitoneally with oxaliplatin at 10 mg/kg/week combined with a daily oral dose of the Costus extract for six weeks. Results: Data from the current study revealed that the extract lowered the toxic effect of oxaliplatin on the testicular tissue samples. This was evident by the significant rise in the serum of total & free testosterone and CD4 cells, and the levels of GSH, SOD and CAT activities in the testis coupled with a marked reduction of serum TNF-α and IL-1β and testis MDA, nitric oxide levels and DNA fragmentation. Also, the extract promoted the regeneration of the histopathological structure of the testis. Conclusion: This study proposes a novel therapeutic application for the Costus extract as a therapeutic agent against testicular toxicity induced by oxaliplatin treatment through its promising anti-inflammatory and antioxidant properties.

This study was conducted to elucidate the possible protective efficiency of Echinacea purpurea hydroethanolic extract (EchEE) against bifenthrin (BIF)-induced neuro-chemical and behavioral changes in rats. Total phenolics content, reducing power and radical scavenging activity of EchEE were estimated. Four groups of adult male albino rats were used (10 rats each) as follows: 1) Control healthy rats ingested with placebo, 2) Healthy rats orally received EchEE (465 mg/kg/day), 3) Rats intoxicated with BIF (7mg/kg/day) dissolved in olive oil, and 4) Rats co-treated with EchEE (465 mg/kg/day) besides to BIF (7mg/kg/day) intoxication. After 30 days, some neuro-chemical and behavioral tests were assessed. The behavioral tests revealed that rats received BIF exhibited exploratory behavior and spatial learning impairments, memory and locomotion dysfunction, and enhanced anxiety level. Biochemical findings revealed that BIF induced-oxidative stress in the cortex and hippocampus; this was appeared from the significant rise in malondialdehyde (MDA) and nitric oxide (NO) levels, coupled with decreased catalase (CAT), superoxide dismutase (SOD), paraoxonase-1 (PON-1) activities, and reduced glutathione (GSH) level in both brain areas. Also, BIF induced a significant increase caspas-3, tumor necrosis factor alpha (TNF), and interleukin-1beta (IL-1ß) in both areas; dopamine and serotonin levels, and ACh-ase activity were markedly decreased in both areas. Interestingly, treatment of rats with EchEE in combination with BIF resulted in a significant decrease in oxidative stress damage, and modulation of the apoptotic and pro-inflammatory markers. Also, EchEE markedly improved behavioral activities and neurotransmitters level that were impaired by BIF. In conclusion, the present study clearly indicated that EchEE can attenuate brain dysfunction induced by pesticides exposure through preventing the oxidative stress. This may be attributed to its high antioxidant component.

Background: Bisphenol A (BPA) causes environmental pollution and is used as a natural antioxidant to protect against chemical side-effects. Costus is a well-known medicinal plant containing several biologically active compounds. We investigated the protective effects of costus extract against the toxic effects of BPA in the rat testes. Results: Biochemical and immunohistochemical investigations revealed that bisphenol reduced the activity of antioxidant enzymes and plasma testosterone levels and significantly increased P53. Co-administration of costus root extract with BPA improved the depletion of antioxidant enzymes, returned testosterone to normal levels, and improved P53 alternations. Histological and ultrastructural examinations showed that BPA reduced body and testicular weights, and the degeneration of seminiferous tubule germ cells, and the use of costus root extract with BPA attenuated these toxic effects. Conclusions: Costus protects rat testes against the toxic effects of BPA.