Rosmarinic acid having potential anti-inflammatory and free radical scavenging activity. We examined the chemotherapeutic effect of rosmarinic against cisplatin (CIS)-induced ovarian toxicity via modulation of oxidative stress and inflammation.Swiss BALB mice used in experimental protocol and mice were divided into different groups. Intraperitoneal injection of CIS (7 mg/kg) was used for ovarian cancer induction. The rats were received rosmarinic acid (2.5, 5, and 10 mg/kg, body weight) treatment for 22 weeks. Body weight, ovary weight food, and water intake were estimated at regular time intervals. Hormonal and antioxidant parameters were estimated in the ovary tissue and serum at the end of the study. Cytokines, inflammatory, and apoptosis parameters were determined at the end of the study.Finally, the ovary tissue histopathology was performed at end of the experimental study. Rosmarinic acid significantly (p < 0.001) improved the body weight and reduced the ovary weight. Rosmarinic acid considerably reduced the hormonal assay parameters, such as antimullerian hormone, estradiol, luteinizing hormone, and follicle-stimulating hormone compared to model control mice. Rosmarinic treatment significantly (p < 0.001) reduced the level of nitric oxide, myeloperoxidase, and boosted the level of antioxidant parameters, such as glutathione, superoxide dismutase, catalase, and glutathione peroxidase in serum and ovary tissue. Rosmarinic acid downregulated the cytokines like interleukin-6, tumor necrosis factor-α, interleukin-1β; inflammatory parameter includes prostaglandin E 2 , cyclooxygenase-2, and inducible nitric oxide synthase at a dose-dependently. Ovary tissue histopathology showed improvement after rosmarinic acid treatment. The result suggests that rosmarinic acid is a protective effect in ameliorating CIS-induced ovary toxicity via alteration of inflammatory and apoptosis parameters.
The purpose of this study was to explore whether and how the Shh pathway exert a neuroprotective effect in SCI. The SCI model of rat was established by a Allen's weight-drop method. Thirty rats were divided into 5 groups as follows: Control, Sham, SCI model, SCI + Shh activator, and SCI + Shh inbibitor. Rats in group of Shh activator or inbibitor were administrated with purmorphamine (10 mg/kg) or cyclopamine (10 mg/kg) respectively daily within one week after establishment of SCI model. Scores of BBB and Reuter were evaluated at the time-points of 1st, 3rd, 5th and 7th day. The pathological injury, the levels of IL-1β and TNF-α and the protein and mRNA expressions of Gli1, Shh and Smoothened in spinal cord tissue were assessed on 7th day, respectively. Rat treated with purmorphamine exhibited a significant increase in BBB score in comparison with SCI group. Interestingly, purmorphamine treatment declined SCI-induced increases in the levels of IL-1 β and TNF-α, whereas cyclopamine administration up-regulated their expressions of these inflammatory cytokines. The pyknotic neuronal cells in gray matter area of the spinal cord and the area of cavity in white matter area were reduced in purmorphamine treatment when compared with SCI group, whereas treatment with cyclopamine elicited an opposite changes. In conclusion, this study demonstrated that Shh activator plays an important protective role in the development of SCI in rat model, which might provide a new strategy via targeting Shh pathway to prevent or treat SCI in the future.
Purpose: The Sonic Hedgehog (Shh) pathway plays an important role in neuroinflammation and neurorepairment after neurological injury, but its role in the development of spinal cord injury (SCI) and related mechanisms are not clear. The purpose of this study was to explore whether and how the Shh signaling pathway exert a neuroprotective effect in SCI. Methods: The SCI model of rat was established by a Allen's weight-drop method. Thirty SPF SD rats were divided into 5 groups as follows: Control, Sham, SCI model, SCI + purmorphamine (Shh activator), and SCI + cyclopamine (Shh inbibitor). Rats in group of Shh activator or Shh inbibitor were administrated with purmorphamine (10 mg/kg) or cyclopamine (10 mg/kg) respectively daily within one week after establishment of SCI model. Scores of Basso, Beattie, Bresnahan (BBB) and Reuter were evaluated at the time-points of 1st, 3rd, 5th and 7th day after establishment of SCI model. Rats were sacrificed on 7th day , and the pathological injury, the levels of inflammatory cytokines (IL-1β and TNF-α) and the protein and mRNA expressions of Gli1, Shh and Smoothened in spinal cord tissue were assessed by HE staining, ELISA, Western Blot and RT-qPCR, respectively.Results: Rat treated with purmorphamine exhibited a significant increase in BBB score in comparison with SCI group, whereas there was no significant difference after cyclopamine treatment. Interestingly, purmorphamine treatment declined SCI-induced increases in the levels of inflammatory cytokines (IL-1 β and TNF-α), whereas cyclopamine administration up-regulated their expressions of these inflammatory cytokines. The pyknotic neuronal cells in gray matter area of the spinal cord and the area of cavity in white matter area were reduced in purmorphamine treatment when compared with SCI group, whereas treatment with cyclopamine elicited an opposite changes. When compared with Sham group, the protein and mRNA expressions of Gli1, Shh, Smoothened were up-regulated in SCI group; whereas these SCI-induced expressions were further activated or inhibited by purmorphamine or cyclopamine treatment.Conclusion: We demonstrated that Shh activator plays an important protective role in the development of SCI in rat model, which might provide a new strategy via targeting Shh pathway to prevent or treat SCI in the future.
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