News Release

Trigonelline exerts its neuroprotective effects in experimental spinal cord injury through modulation of inflammation, apoptosis, and neurotrophic factors

Peer-Reviewed Publication

Higher Education Press

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Effect of trigonelline on the plantar test (A), paw pressure test (B), von-Frey hair test (C), tail immersion test (D), grip strength test (E) and motor nerve conduction velocity (F). Data are expressed as mean±SEM (n=6) and were analyzed using two-way ANOVA, followed by Bonferroni's multiple range test for post-hoc comparisons. #P<0.05 compared to the normal group, &P<0.05 compared to the sham group, *P<0.05 compared to the SCI group. MP30: methylprednisolone 30 mg/kg; N: normal; S: sham; SCI: Spinal cord injury; T50: trigonelline 50 mg/kg, T100: trigonelline 100 mg/kg, T200: trigonelline 200 mg/kg.

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Credit: Ye ZL, Cao Y

Although certain treatment methods have shown beneficial clinical effects, no definitive cure exists for spinal cord injury (SCI). Exploring new therapies and interventions with complementary and alternative medicines to manage SCI is necessary to achieve promising efficacy and fewer side effects in individuals. Trigonelline shows promise in alleviating various neurological disorders. This study aimed to assess the neuroprotective effects of trigonelline in a surgical aneurysm clip-induced-SCI rat model through behavioral, biochemical, and histological assessments.
Rats (Sprague-Dawley, male) were randomly assigned to seven groups (n=15 per group): normal, sham, SCI control (1% DMSO), methylprednisolone (30 mg/kg), and trigonelline (50, 100, and 200 mg/kg). Rats received respective treatment daily for 28 days. SCI was induced by using a temporary aneurysm clip. Behavioral, biochemical, and histological analyses were performed to investigate the neuroprotective effect of trigonelline. 
Trigonelline (100 and 200 mg/kg) treatment effectively (P<0.05) mitigated SCI-induced changes in mechano-tactile sensation, allodynia, hyperalgesia, and motor nerve conduction velocity. It notably (P<0.05) downregulated apoptotic (Bax and caspase-3) and inflammatory (COX-Ⅱ) markers, while upregulating Bcl-2 and BDNF mRNA expression in the spinal cord (P<0.05). Furthermore, trigonelline effectively alleviated (P<0.05) SCI-induced alterations in mitochondrial complex levels, resulting in enhanced nicotinamide adenine dinucleotide dehydrogenase, succinate dehydrogenase, redox activity, and cytochrome-C levels. Histological examination of spinal cord tissue indicated that trigonelline significantly (P<0.05) ameliorated the histological damage caused by SCI, thereby improving neuronal degeneration, inflammatory cell infiltration, and necrosis. 
Trigonelline shows neuroprotective properties in SCI rats by reducing allodynia, hyperalgesia, and inflammation, stabilizing mitochondrial enzyme complexes, and modulating apoptotic and neurotrophic factors. Thus, trigonelline holds promise as a potential neuroprotective agent.
The work entitled “Trigonelline exerts its neuroprotective effects in experimental spinal cord injury through modulation of inflammation, apoptosis, and neurotrophic factors” was published on Asian Pacific Journal of Tropical Biomedicine (published on Jan. 17, 2025).

DOI: 10.4103/apjtb.apjtb_519_24


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