Chebulic acid attenuates ischemia reperfusion induced biochemical alteration in diabetic rats

Silawat, Narendra; Gupta, Vipul

doi:10.3109/13880209.2012.698288

Cited by 15 publications

(9 citation statements)

References 37 publications

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“…or vehicle (40% ethanol). This dose is common in the literature 11, 12 and is considerably less than the 500 mg/kg/day used in the original assessment of glyburide’s ability to inhibit NLRP3. 8 The glyburide was prepared by suspending 5 mg/ml in 100% ethanol at 56 °C with occasional vortexing until dissolved.…”

Section: Methodsmentioning

confidence: 99%

The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction

et al. 2016

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Purpose While bladder outlet obstruction (BOO) is well-established to elicit an inflammatory reaction in the bladder that leads to overactive bladder and fibrosis, little is known about the mechanism by which this is initiated. Nod-Like Receptors (NLRs) and the structures they form (inflammasomes) have been identified as sensors of cellular damage (including pressure-induced damage) and triggers of inflammation. Recently, we identified these structures in the urothelium. In this study we assess the role of the NLRP3 inflammasome in the bladder dysfunction resulting from BOO. Materials and Methods BOO was created in female rats by insertion of a 1 mm (o.d.) transurethral catheter, tying a silk ligature around the urethra and removing the catheter. Untreated and sham-operated rats served as controls. BOO rats were given vehicle (10% ethanol) or 10 mg/kg of glyburide (an NLRP3 inhibitor; daily for 12 days, p.o.). Inflammasome activity, bladder hypertrophy, inflammation and bladder function (urodynamics) were assessed. Results: BOO increased urothelial inflammasome activity, bladder hypertrophy, and inflammation and reduced voiding volume. Glyburide blocked inflammasome activation, reduced hypertrophy and prevented inflammation. The reduction in void volume was also attenuated by glyburide, mechanistically by an increase in the duration of detrusor contraction and voiding period. Conclusion The results suggest the importance of the NLRP3 inflammasome in the induction of inflammation and bladder dysfunction secondary to BOO. Arresting these processes with NLRP3 inhibitors may prove useful in treating the symptoms they produce.

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Section: Methodsmentioning

confidence: 99%

The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction

et al. 2016

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“…which have free radical scavenging activity and might be used for reducing oxidative stress in diabetes [35]. Upon investigating the protective activity of Terminalia chebula extract against AGE-induced vascular endothelium dysfunction, human umbilical vein endothelial cells (HUVEC) incubated with 100 µg/mL of AGEs had significantly enhanced reactive oxygen species (ROS) formation, whereas the treatment of T. chebula reduced AGE-induced ROS generation [36]. Chebulic acid at both doses (25 and 50 mg/kg) improves biochemical alterations caused by renal ischemia in diabetic rats [37].…”

Section: Discussionmentioning

confidence: 99%

Unique Therapeutic Approach of Tab.Dibet-All (A Poly Herbomineral Formulation), Tab.Dtox-OD and Tab.Glybra in a Newly Diagnosed Case of Type-2 Diabetes Mellitus. A Case Report

Giri¹

2018

Endocrinol Metab Syndr

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Along with all the commonly known rationale; oxidative stress, reactive oxygen species (ROS), growing number of AGEs, accumulation and outbreak of Tridoshas. Throughout year plays decisive role in the development of Diabetes as well as its complications. In the present study, I have discussed about their effective and economical management based on the principles of Ayurveda in the form of distinctive line of treatment which includes Tab.Dibet-all (a poly herbomineral formulation), Tab. Dtox-OD and Tab Glybra. This trio is indistinguishable from allopathy drugs in terms of pharmacology. With so many benefits concealed inside; this line of treatment is having remarkable potential regarding antidibetic, antiglycating, antihyperlipidimic, rejuvinative and preventive/protective activities by the means of breaking cross-links of proteins induced by AGEs, inhibition of AGE formation, blockade of the AGE-RAGE interaction, suppression of RAGE expression and prevention from glycer-AGEs-induced ROS formation ensuring good control over intricate pathology of diabetes and thus protecting diabetics to a higher extent from the complications of diabetes slowly footing towards them. This is the most imperative thing regarding intricate and vague pathology like Diabetes mellitus Only the integrated approach towards this gruesome situation will going to help mankind. May this study of 'Tab. Dibet-all (a poly herbomineral formulation), Tab. Dtox-OD and Tab. Glybra' with its sovereign effects could serve as a light of hope towards search of ideal treatment of Diabetes mellitus type-2. This can be a supplementary remedy for type-1, hereditary and chronic diabetics also and unquestionably lend a hand to revolutionize the future scenario of these tribulations.

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“…T . chebula and its constituents possesses cytoprotective activity against various oxidative stress-mediated pathological conditions such as brain ischemia, renal reperfusion injury, gastric ulcer, burn wounds, and drug-induced hepatotoxicity 16 46 47 48 49 . Based on earlier pharmacological and biochemical studies, this plant exhibits antioxidant and free radical-scavenging activities in vitro and in vivo 18 19 .…”

Section: Discussionmentioning

confidence: 99%

Terminalia Chebula provides protection against dual modes of necroptotic and apoptotic cell death upon death receptor ligation

Lee

Byun

Seok

et al. 2016

Sci Rep

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Death receptor (DR) ligation elicits two different modes of cell death (necroptosis and apoptosis) depending on the cellular context. By screening a plant extract library from cells undergoing necroptosis or apoptosis, we identified a water extract of Terminalia chebula (WETC) as a novel and potent dual inhibitor of DR-mediated cell death. Investigation of the underlying mechanisms of its anti-necroptotic and anti-apoptotic action revealed that WETC or its constituents (e.g., gallic acid) protected against tumor necrosis factor-induced necroptosis via the suppression of TNF-induced ROS without affecting the upstream signaling events. Surprisingly, WETC also provided protection against DR-mediated apoptosis by inhibition of the caspase cascade. Furthermore, it activated the autophagy pathway via suppression of mTOR. Of the WETC constituents, punicalagin and geraniin appeared to possess the most potent anti-apoptotic and autophagy activation effect. Importantly, blockage of autophagy with pharmacological inhibitors or genetic silencing of Atg5 selectively abolished the anti-apoptotic function of WETC. These results suggest that WETC protects against dual modes of cell death upon DR ligation. Therefore, WETC might serve as a potential treatment for diseases characterized by aberrantly sensitized apoptotic or non-apoptotic signaling cascades.

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Chebulic acid attenuates ischemia reperfusion induced biochemical alteration in diabetic rats

Cited by 15 publications

References 37 publications

The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction

The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction

Unique Therapeutic Approach of Tab.Dibet-All (A Poly Herbomineral Formulation), Tab.Dtox-OD and Tab.Glybra in a Newly Diagnosed Case of Type-2 Diabetes Mellitus. A Case Report

Terminalia Chebula provides protection against dual modes of necroptotic and apoptotic cell death upon death receptor ligation

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