Drug · Succinate semialdehyde dehydrogenase inhibitor
4 linked trials carry an injury-indication flag. These flags support record-level exploration and sit alongside the stringent aggregate counts described in Methods.
Acute Kidney Injury · Ischemia Reperfusion Injury
Enrolment: 0 · Results not recorded
Acute Kidney Injury · Ischemia Reperfusion Injury
Enrolment: 0 · Results not recorded
Shock, Hemorrhagic
Enrolment: 59 · Results not recorded
Shock, Hemorrhagic · Trauma
Enrolment: 1 · Results not recorded
PTSD
Enrolment: 101 · Results not recorded
Cardiac Valve Disease · Coronary Artery Disease · Organ Failure, Multiple
Enrolment: 122 · Results not recorded
7 studies reported at therapy level; 9 evidence entries itemised.
Model: Doxorubicin-induced acute cardiotoxicity
The greatest biochemical and histopathological improvement was seen in the group receiving mesenchymal stem cells together with sodium valproate and electrical stimulation, indicating that electric fields and valproate enhance homing of the cells to doxorubicin-damaged myocardium.
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Model: Needle penetration trauma of whole brain tissue caused by intracranial cannula placement and intracerebral injection
Acute intracerebral injection of the VPA-PEG conjugate increased virtually all assayed phospho-proteins including well known pro-survival factors despite the procedural needle trauma, whereas unmodified valproic acid decreased signalling over the same hour
Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.55. Machine-extracted fields require source verification.
Model: Laminectomy at L4 with silicone gel implantation into the epidural space at L5 and L6 producing cauda equina compression
Valproic acid significantly improved lower limb motor function, reduced Wallerian degeneration and demyelinating lesions with increased myelination, and decreased apoptotic neuron counts in the spinal cord anterior horn and dorsal root ganglia relative to saline controls.
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Model: Chronic compressive spinal cord injury
Valproic acid inhibited neural stem/precursor cell proliferation but promoted neuronal and reduced astrocytic differentiation, increased newborn and mature neuron markers in the injured cord and improved BBB scores, although corticospinal tracts were not significantly improved.
Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.6. Machine-extracted fields require source verification.
Model: Spinal cord contusion injury, with outcomes followed for 12 weeks and tissue analysed 3 months post-injury
Valproic acid-treated contused rats showed significantly greater reductions in cavitation, H/M ratio and GFAP expression and higher Basso-Beattie-Bresnahan scores than untreated animals (P < 0.05). The optimal regimen was 300 mg/kg given 12 h after injury, which produced the greatest increase in lo…
Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.75. Machine-extracted fields require source verification.
Model: Severe controlled cortical impact, isolated traumatic brain injury, animals killed 6 h after injury
Traumatic brain injury increased serum syndecan-1 at 3 and 6 h. Valproic acid reduced lesion size (40.45 mm versus 59.57 mm, p = 0.023) but was associated with greater glycocalyx shedding at 3 h, and syndecan-1 correlated inversely with lesion size.
Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.85. Machine-extracted fields require source verification.
Model: Traumatic brain injury in adult rats, acute phase; the specific injury model is not stated in the abstract
Valproic acid given after traumatic brain injury attenuated brain oedema, contusion volume and neuronal apoptosis and partly blocked the rise in caspase-3 activity, with the benefit reduced by ERK or Akt inhibition.
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Extraction: not specified. Machine-extracted fields require source verification.
Extraction: mesh. Machine-extracted fields require source verification.
