We investigated the wound healing efficacy of the Foeniculum vulgare compounds, fenchone and limonene, using an excisional cutaneous wound model in rats. An excision wound was made on the back of the rat and fenchone and limonene were applied topically to the wounds once daily, separately or together, for 10 days. Tissue sections from the wounds were evaluated for histopathology. The healing potential was assessed by comparison to an untreated control group and an olive oil treated sham group. We scored wound healing based on epidermal regeneration, granulation tissue thickness and angiogenesis. After day 6, wound contraction with limonene was significantly better than for the control group. Ten days after treatment, a significant increase was observed in wound contraction and re-epithelialization in both fenchone and limonene oil treated groups compared to the sham group. Groups treated with fenchone and with fenchone + limonene scored significantly higher than the control group, but the difference was not statistically significant compared to the olive oil treated group. Our findings support the beneficial effects of fenchone and limonene for augmenting wound healing. The anti-inflammatory and antimicrobial activities of fenchone and limonene oil increased collagen synthesis and decreased the number of inflammatory cells during wound healing and may be useful for treating skin wounds.
Objective: The aim of this study was to investigate the effects of naringin, a known flavonoid, on in vitro cytotoxicity, irritation and in vivo potential efficacy when topically applied to the diabetic wound. Material and Method: In vitro direct contact assay and hen's egg chorio-allantoin membrane tests were used to evaluate irritation, and cytotoxicity potential of Naringin. In vitro antimicrobial activity was also tested. Topical treatments were administered once a day on the wound. Wound lesions were photographed and statistically analyzed. After the 10th day, histopathological parameters of tissues were assessed.
Objective: In this study, the possible central antinociceptive activity of beta-sitosterol is investigated along with its association of stimulation of opioidergic, serotonergic, adrenergic, and cholinergic receptors to mice central analgesia because of the beta-sitosterol administration.Material and Method: The beta-sitosterol was administrated to mice in various doses, such as 5, 10 and 20 mg/kg. Then, the mice analyzed via hot-plate and tail-flick assay to investigate the possible antinociceptive effects of beta-sitosterol. Additionally, in order to associate the mechanism of action mechanism, 20 mg/kg of beta-sitosterol was intraperitoneally administered to the animal which were previously pre-treated with opioid antagonist naloxone (5 mg/kg), serotonin 5-HT2A/2C receptor antagonist ketanserin (1 mg/kg), serotonin 5-HT3 receptor antagonist -ondansetron (1 mg/kg), α2-adrenoceptor antagonist yohimbine (1 mg/kg) and muscarinic antagonist atropine (5 mg/kg), as well as nicotinic antagonist mecamylamine (1 mg/kg).Result and Discussion: The antinociceptive effect of beta-sitosterol was confirmed as dose-dependent for 5, 10, and 20 mg/kg doses in tail-flick and hot-plate tests. It can be concluded that beta-sitosterol promotes central antinociception effects associated with the spinal and supraspinal mediated cholinergic and opioidergic modulation.
The clinical use of cisplatin, which is a first-line anticancer agent, is highly restricted due to its adverse effects on kidneys that lead to nephrotoxicity. Therefore, some potential reno-protective substances have been used in combination with cisplatin to cope with nephrotoxicity. Due to its high antitumor activity and oxygen-carrying capacity, we investigated the molecular effects of squalene against cisplatin-induced oxidative stress and kidney damage in mice. Single dose of cisplatin (7 mg/kg) was given to male Balb/c mice. Squalene (100 mg/kg/day) was administered orogastrically to mice for 10 days. Following sacrification, molecular alterations were investigated as analysis of the levels of oxidative stress index (OSI), inflammatory cytokines and cell survival-related proteins in addition to histopathological examinations in mice kidney tissue. The level OSI and Interferon-gamma (IFN-γ) decreased in the cisplatin and squalene cotreated mice compared to cisplatin-treated mice. Squalene treatment also increased the activation of protein kinase B (AKT). Furthermore, cisplatin-induced inactivation of mammalian target of rapamycin (mTOR) and histopathological damages were reversed by squalene. It may be suggested that squalene ameliorated the cisplatin-induced histopathological damages in the kidney through activation of AKT/mTOR signaling pathway by regulating the balance of the redox system due to its antioxidative effect.
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