Mitochondrial Permeability Transition Pore-as a Promising Target for Novel Neuroprotective Agents

Бачурин, С. О.

doi:10.4172/2155-983x.1000e143

Cited by 2 publications

(1 citation statement)

References 13 publications

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“…Viability of the mitochondrial is dependent on mitochondrial permeability transition (mPT), which refers to a sudden increase in permeability of the inner mitochondrial membrane (IMM) to solutes of molecular mass less than 1500 Da [1,2]. There are evidences indicating that mPT is a focal point in mediating cardiac dysfunction and cell death [3,4].…”

Section: Introductionmentioning

confidence: 99%

Methanol Fraction of Daniellia oliveri (ROLFE) Leaves Induces Mitochondrial-mediated Apoptosis in Rats via Alteration of Liver Mitochondrial Viability

Achem,

Onyiba,

Banwo

et al. 2023

Preprint

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Background: Alteration of mitochondrial viability by induction of mitochondrial permeability transition (mPT) brings about mitochondrial-mediated apoptosis. D. oliveri is a medicinal plant traditionally used for the management of certain ailments including tumours. Purpose: Investigating effects of Methanol Fraction of D. oliveri Leaves (MFDO) on mitochondrial-mediated apoptosis. Methods: Twenty-four male rats (70-90 g) were grouped into 4 according to intraperitoneal treatments (14 days): control (distilled water), 50, 100 and 200 mg/kg MFDO. The mitochondrial ATPase and DNA fragmentation were assayed by spectrophotometry. Apoptotic biomarkers were assayed by immunohistochemistry. Caspases-3 and -9 were assessed using ELISA. GC-MS was employed to identify compounds in MFDO. Results: MFDO exhibited invitro antioxidant properties through inhibition of DPPH and ferric radicals. There was induction of mPT by 50, 100 and 200 mg/kg MFDO relative to control. Furthermore, MFDO inhibited mLPO and enhanced mATPase relative to control. Expression of Bax, p53 and cytochrome c proteins were up-regulated, while Bcl-2 protein expression was down-regulated. Caspase-3 and -9 activities were enhanced, and DNA fragmentation was induced. GC-MS of MFDO revealed the presence of apoptosis-inducing compounds. Conclusion: MFDO induces mitochondrial-mediated apoptosis via alteration of rats liver mitochondrial viability. MFDO is therefore relevant for drug development against diseases.

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