Gene expression regulation of Bcl2, Bax and cytochrome-C by geraniol on chronic MPTP/probenecid induced C57BL/6 mice model of Parkinson’s disease

Esculetin induces apoptosis in human gastric cancer cells through a cyclophilin D-mediated mitochondrial permeability transition pore associated with ROS

“…Second, esculetin dosedependently enhanced the expression of Bax and Bak (proapoptotic regulatory proteins), down-regulated the expression of Bcl-2 and Bcl-xL (anti-apoptotic regulatory proteins), and induced cytochrome c release from the mitochondria into the cytoplasm. The fate of the cell is determined at the mitochondrial membrane by the balance between the pro-apoptotic (Bax and Bak) and antiapoptotic (Bcl2 and Bcl-xL) members of the Bcl2 family in the mitochondrial pathway [39,40]. Third, esculetin caused a dramatic decrease of the MMP, which could be blocked by CsA, an agent that prevents the opening of MPTP by binding to CypD.…”

Chronic MPTP treatment produces hyperactivity in male mice which is not alleviated by concurrent trehalose treatment

“…This may appear somewhat surprising as the majority of the chronic MPTPp paradigm literature has reported either a lack of MPTPp effects [46] or hypoactivity (e.g., [9,12,16,47]). That hypoactivity seems apparent whether the assessment is conducted shortly after the last MPTPp injection (e.g., [12]) or up to 11 weeks post-treatment (e.g., [16]). However, MPTPp-induced hyperactivity as measured by distance traveled was replicated in both experiments of the current study.…”

“…For example, when assessed within 48 h of the last MPTP treatment, male mice exhibit increased latencies in pole descent, decreased latencies to remain on a rotating rod, decreased locomotor activity, increased foot faults during beam crossing or grid tests, poor swimming ability, increased tail suspension immobility, increased akinesia and catalepsy, memory impairments in an avoidance task, and olfactory deficits [3,[6][7][8][9][10][11][12]. Similar treatment has also been described to cause long-lasting impairments (up to 6 months post-treatment) on latencies to remain on a rotating rod [2,13,14], in foot slips or gait alterations [15,16], on performance of the cued, but not spatial, version of a water maze task [16], and on baseline and amphetamine-induced locomotor activity [16].…”

Neuroprotective effects of geniposide in the MPTP mouse model of Parkinson's disease

“…Apoptosis is known to be an important factor related to the loss of nigral dopaminergic neurons in PD, which can be assessed by analysing the expression of apoptotic proteins (Bcl-2, Bax, Pro-caspase3 and Cleaved-caspase3) by Western blot (Rekha and Selvakumar, 2014;Sharma et al, 2013). The Western blot analysis showed that the expression of anti-apoptotic signaling molecule Bcl-2 was reduced by MPTP treatment (P < 0.001), expression of the pro-apoptotic signaling molecule Bax was increased by MPTP treatment (P < 0.001), and the ratio of Bcl-2/Bax was decrease (P < 0.001), compared with control group.…”