Troxerutin exerts neuroprotection in 6-hydroxydopamine lesion rat model of Parkinson’s disease: Possible involvement of PI3K/ERβ signaling

Baluchnejadmojarad, Tourandokht; Jamali-Raeufy, Nida; Zabihnejad, Sedigheh; Rabiee, Navid; Roghani, Mehrdad

doi:10.1016/j.ejphar.2017.03.002

Cited by 41 publications

(25 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The body weight of mice was assessed daily prior to administration of the administered treatment to confirm the experimental model of 5-FU induced intestinal mucositis. The TRX doses considered in the current study are in accordance with those in previous published studies [19][20][21][22]61]. daily prior to administration of the administered treatment to confirm the experimental model of 5-FU induced intestinal mucositis.…”

Section: Experimental Protocol Of 5-fu-induced Intestinal Mucositissupporting

confidence: 69%

“…daily prior to administration of the administered treatment to confirm the experimental model of 5-FU induced intestinal mucositis. The TRX doses considered in the current study are in accordance with those in previous published studies [19][20][21][22]61]. To investigate the role of cyclooxygenase 2 (COX-2) enzyme during TRX treatment of 5-FUinduced intestinal mucositis, COX-2 was blocked by an intraperitoneal (i.p) injection of 7.5 mg/kg of CLX.…”

Section: Experimental Protocol Of 5-fu-induced Intestinal Mucositismentioning

confidence: 86%

“…Troxerutin (TRX) is a semi-synthetic flavonoid, derived from rutin, which is extracted from Dimorphandra gardneriana. This compound has various pharmacological activities, including antioxidant [17][18][19], anti-inflammatory [20], anti-apoptotic [21,22], and antiedematogenic [23,24]. Further, it is a potent therapeutic agent for neuropathic pain [25].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Troxerutin Prevents 5-Fluorouracil Induced Morphological Changes in the Intestinal Mucosa: Role of Cyclooxygenase-2 Pathway

et al. 2020

View full text Add to dashboard Cite

Intestinal mucositis is a common complication associated with 5-fluorouracil (5-FU), a chemotherapeutic agent used for cancer treatment. Troxerutin (TRX), a semi-synthetic flavonoid extracted from Dimorphandra gardneriana, has been reported as a potent antioxidant and anti-inflammatory agent. In the present study, we aimed to evaluate the effect of TRX on 5-FU-induced intestinal mucositis. Swiss mice were randomly divided into seven groups: Saline, 5-FU, TRX-50, TRX-100, TRX-150, Celecoxib (CLX), and CLX + TRX-100. The weight of mice was measured daily. After treatment, the animals were euthanized and segments of the small intestine were collected to evaluate histopathological alterations (morphometric analysis), levels of malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), mast and goblet cell counts, immunohistochemical analysis, and cyclooxygenase-2 (COX-2) activity. Compared to the saline treatment, the 5-FU treatment induced intense weight loss and reduction in villus height. TRX treatment (100 mg/kg) prevented the 5-FU-induced histopathological changes and decreased oxidative stress by decreasing the MDA levels and increasing GSH concentration. TRX attenuated inflammatory process by decreasing MPO activity, intestinal mastocytosis, and COX-2 expression. TRX also reversed the depletion of goblet cells. Our findings suggest that TRX at a concentration of 100 mg/kg had chemopreventive effects on 5-FU-induced intestinal mucositis via COX-2 pathway.

show abstract

Section: Experimental Protocol Of 5-fu-induced Intestinal Mucositissupporting

confidence: 69%

Section: Experimental Protocol Of 5-fu-induced Intestinal Mucositismentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Troxerutin Prevents 5-Fluorouracil Induced Morphological Changes in the Intestinal Mucosa: Role of Cyclooxygenase-2 Pathway

et al. 2020

View full text Add to dashboard Cite

show abstract

“…MiR-27b IN transfection reduced the LDH release and cell apoptosis after FS stimulation in PC12 cells, suggesting that miR-27b inhibition protects PC12 cells from the neurotoxicity of iron. Moreover, miR-27b IN transfection attenuated the FS-induced increase in ROS production, Tnf expression and MDA content, which is another OS marker that directly reflects the extent of lipid peroxidation [ 47 ]. Nrf2 knockdown blocked the protective effects of miR-27b inhibition, strongly suggesting the Nrf2/ARE pathway is essential for the protective effects of miR-27b inhibition on the iron-induced oxidative and inflammatory damage to PC12 cells.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-27b inhibition promotes Nrf2/ARE pathway activation and alleviates intracerebral hemorrhage-induced brain injury

Liu

et al. 2017

Oncotarget

View full text Add to dashboard Cite

Oxidative stress and neuroinflammation are the key factors leading to secondary brain injury after intracerebral hemorrhage (ICH). We investigated the effects of miR-27b, an oxidative stress-responsive microRNA, on ICH-induced brain injury in rats. The ICH model was induced by intracerebral injection of collagenase. Following ICH, miR-27b expression in the striatum was reduced, whereas expression of Nrf2 mRNA and protein was increased. In PC12 cells, overexpression of miR-27b reduced expression of Nrf2, Hmox1, Sod1 and Nqo1, while miR-27b inhibition had the opposite effects. Dual luciferase reporter assays showed that Nrf2 mRNA was a direct target of miR-27b. Intracerebroventricular injection of miR-27b antagomir and transfection of miR-27b inhibitor inhibited endogenous miR-27b in rats and PC12 cells, respectively. MiR-27b antagomir promoted activation of the ICH-induced Nrf2/ARE pathway and reduced the lipid peroxidation, neuroinflammation, cell death and neurological deficits otherwise seen after ICH. In PC12 cells, the miR-27b inhibitor diminished iron-induced oxidative stress, inflammation and apoptosis, and those effects were blocked by Nrf2 knockdown. These results demonstrate that miR-27b inhibition alleviates ICH-induced brain injury, which may be explained in part by its regulation on the Nrf2/ARE pathway.

show abstract

“…Our data demonstrated a key involvement of GPR30 and/or ERβ in the neuroprotective and anti-apoptotic actions of the phytoestrogens daidzein and genistein [ 53 , 54 ]. Similarly, ERβ signalling has been linked to flavonoid troxerutin-induced mitigation of apoptosis in a 6-hydroxydopamine-induced lesion rat model for PD [ 55 ]. In addition, we provided evidence for a crucial role of ERα in the neuroprotective function of raloxifene during hypoxia [ 56 ].…”

Section: Interactions Of Apoptosis and Autophagy With Steroid And mentioning

confidence: 99%

Steroid and Xenobiotic Receptor Signalling in Apoptosis and Autophagy of the Nervous System

Wnuk

Kajta

2017

IJMS

View full text Add to dashboard Cite

Apoptosis and autophagy are involved in neural development and in the response of the nervous system to a variety of insults. Apoptosis is responsible for cell elimination, whereas autophagy can eliminate the cells or keep them alive, even in conditions lacking trophic factors. Therefore, both processes may function synergistically or antagonistically. Steroid and xenobiotic receptors are regulators of apoptosis and autophagy; however, their actions in various pathologies are complex. In general, the estrogen (ER), progesterone (PR), and mineralocorticoid (MR) receptors mediate anti-apoptotic signalling, whereas the androgen (AR) and glucocorticoid (GR) receptors participate in pro-apoptotic pathways. ER-mediated neuroprotection is attributed to estrogen and selective ER modulators in apoptosis- and autophagy-related neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases, stroke, multiple sclerosis, and retinopathies. PR activation appeared particularly effective in treating traumatic brain and spinal cord injuries and ischemic stroke. Except for in the retina, activated GR is engaged in neuronal cell death, whereas MR signalling appeared to be associated with neuroprotection. In addition to steroid receptors, the aryl hydrocarbon receptor (AHR) mediates the induction and propagation of apoptosis, whereas the peroxisome proliferator-activated receptors (PPARs) inhibit this programmed cell death. Most of the retinoid X receptor-related xenobiotic receptors stimulate apoptotic processes that accompany neural pathologies. Among the possible therapeutic strategies based on targeting apoptosis via steroid and xenobiotic receptors, the most promising are the selective modulators of the ER, AR, AHR, PPARγ agonists, flavonoids, and miRNAs. The prospective therapies to overcome neuronal cell death by targeting autophagy via steroid and xenobiotic receptors are much less recognized.

show abstract

Troxerutin exerts neuroprotection in 6-hydroxydopamine lesion rat model of Parkinson’s disease: Possible involvement of PI3K/ERβ signaling

Cited by 41 publications

References 47 publications

Troxerutin Prevents 5-Fluorouracil Induced Morphological Changes in the Intestinal Mucosa: Role of Cyclooxygenase-2 Pathway

Troxerutin Prevents 5-Fluorouracil Induced Morphological Changes in the Intestinal Mucosa: Role of Cyclooxygenase-2 Pathway

MicroRNA-27b inhibition promotes Nrf2/ARE pathway activation and alleviates intracerebral hemorrhage-induced brain injury

Steroid and Xenobiotic Receptor Signalling in Apoptosis and Autophagy of the Nervous System

Contact Info

Product

Resources

About