Antiinflammatory effects of phenolic compounds from Emblica officinalis were evaluated in carrageenan and cotton pellet induced acute and chronic inflammatory animal model. Fractions of E. officinalis containing free (FPEO) and bounded (BPEO) phenolic compounds were assessed by HPLC technique. The free and bound phenolic compounds were studied for their acute and chronic antiinflammatory activity at dose level of 20 and 40 mg/kg. The carrageenan induced acute inflammation was assessed by measuring rat paw volume at different time of intervals. Further, cotton pellet induced chronic inflammation was assessed by granulomatous tissue mass estimation along with the estimation of tissue biomarker changes (i.e. lipid peroxidation, reduced glutathione, myeloperoxidase and plasma extravasation). The results indicated that in both acute and chronic inflammation, FPEO and BPEO show reduction in the inflammation, but significant effects was observed only at high doses of both fractions which was comparable to diclofenac treated group. In conclusion, phenolic compounds of E. officinalis may serve as potential herbal candidate for amelioration of acute and chronic inflammation due to their modulatory action of free radicals.
This study was aimed to evaluate the role of ‰unarizine on gentamicin (GEM) induced nephrotoxicity in rat. Administration of GEM (40 mg/kg, s.c. for 10 consecutive days) signiˆcantly increased blood urea nitrogen (BUN), Nacetyl b-d-glucosaminidase (NAG), thiobarbituric acid reactive substances (TBARS) and total calcium whereas, decreased body weight, fractional excretion of sodium (FrNa), creatinine clearance (CrCl), reduced glutathione (GSH), mitochondrial cytochrome c oxidase (Cyt-C oxidase) and ATP levels resulting in nephrotoxicity. Further, ‰unarizine (100, 200 and 300 mmol/kg, p.o.) was administered to evaluate its renoprotective eŠect against GEM induced nephrotoxicity and the results were compared with cylcosporin A (CsA, 50 mmol/kg, p.o.). Flunarizine resulted in the attenuation of renal dysfunction and oxidative marker changes in rats subjected to GEM induced nephrotoxicity in a dose dependent manner. Medium and higher doses of ‰unarizine produced signiˆcant renal protective eŠect which was comparable to cyclosporin A. The results of this study clearly revealed that ‰unarizine protected the kidney against the nephrotoxic eŠect of GEM via mitochondrial permeability transition pore (MPTP) inactivation potential.
PurposeThe present study was designed to explore the potential of flunarizine for cisplatin induced painful uremic neuropathy in rats.MethodsCisplatin (2 mg/kg; i.p., for 5 consecutive days) was administered and renal uremic markers i.e., serum creatinine were estimated on days 4 and 25. Behavioral changes were assessed in terms of thermal hyperalgesia (hot plate, plantar, tail immersion, and tail flick tests at different time intervals). Biochemical analysis of total calcium, superoxide anion, DNA, and transketolase, and myeloperoxidase activity in tissue samples was also performed. Furthermore, flunarizine (100, 200, and 300 µM/kg; p.o., for 21 consecutive days) was administered to evaluate its potency on uremic neuropathy, and the results were compared with those for the carbamazepine-treated (30 mg/kg; p.o., for 21 consecutive days) groups.ResultsFlunarizine attenuated the cisplatin-induced uremic neuropathy, and the degree of behavioral and biochemical changes in serum and tissue samples in a dose dependent manner. The medium and high doses of flunarizine were shown to produce a significant effect on cisplatin induced painful uremic neuropathy.ConclusionsOur results indicate the potential of flunarizine for anti-oxidative, anti-inflammatory, and neuroprotective actions. Therefore, it may have use as a novel therapeutic agent for the management of painful uremic neuropathy.
This study was aimed to evaluate the protective effect of flunarizine on cisplatin-induced acute renal failure. Administration of cisplatin (6 mg/kg, i.p. on day 6) significantly increased serum blood urea nitrogen and creatinine, urinary N-acetyl β-D-glucosaminidase, tissue thiobarbituric acid reactive substances and total calcium whereas, decreased body weight, fractional excretion of sodium, creatinine clearance tissue-reduced glutathione, mitochondrial cytochrome c oxidase, and ATP levels were observed in acute renal failure rats. Moreover, cisplatin produced histopathological changes in the renal tissue. Furthermore, flunarizine (100, 200, and 300 μM/kg, p.o., for six consecutive days) was administered to evaluate its therapeutic potential in acute renal failure, and the results were compared with cyclosporin A (50 μM/kg, p.o., for six consecutive days) as a reference drug. Flunarizine resulted in the attenuation of cisplatin-induced renal dysfunction, oxidative stress marker, mitochondrial damage, and histopathological changes in rats. Medium and higher doses of flunarizine produced significant renal protective effect which was comparable to cyclosporin A. The results of this study clearly revealed that flunarizine protected the kidney against the nephrotoxic effect of cisplatin via mitochondrial permeability transition pore inactivation potential.
We report the case of a 25-year-old woman with tetralogy of Fallot who presented with chest pain and hypertension, and on further investigation, was diagnosed with a pheochromocytoma in the right adrenal gland. She underwent surgical excision of the tumor. While the simultaneous occurrence of these two diseases is extremely rare, the suspicion of a possible relationship has been raised in the past.
We encountered and reported a case of inadvertent misplacement of a tunneled hemodialysis catheter (tHDC) into azygos arch inserted form right internal jugular vein (RIJV) despite real-time fluoroscopy guidance. We subsequently performed a literature search of Pubmed using the index words of azygos, catheter, hemodialysis, misplace, malposition, and misposition, to study the anatomical and related factors predisposing unintended AV misposition in HD setting. The search was limited to reports in humans and with abstract in English. Results: From 2005 to August 31st, 2018, a total of 11 articles containing 16 cases of misplacement of HDCs into AV were identified. Of the 17 cases of unintentional AV misposition including our presented case, the majority of the HDCs (94.1%, 16/17) were tHDCs and only 1 case was with temporary (untunneled) catheter. Most catheter misplacements (88.2%, 15/17) were performed without real-time radiological guidance. The incidence of inadvertent AV cannulation in different institutions ranged between 0.6 to 3.8%. Among 16 misplaced tHDCs, the incidence rate of AV misposition from RIJV and left internal jugular vein (LIJV) was equally 50%. Conclusions: We present in this article probably the largest case series of HDC misplacement into AV. Based upon anatomical and case studies,we have verified that the vena azygos major joins the posterior aspect of SVC at different directions and levels. Despite relative low incidence, LIJV and RIJV insertion are both susceptible to this complication with a comparable incidence rate. Aside from anatomy, the material and gauge of the catheter,availability of radiological guidance and operator's experience all affect the outcome of CVC placement. Caution is advised to avoid likely pitfalls during HDC placement.
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