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Objective: The mechanisms behind Alzheimer's disease (AD) remain largely unclear. Reactive oxygen species and inflammatory cytokines contribute to inflammation and synaptic dysfunction in AD. This study investigates whether silibinin’s neuroprotective properties act through regulating oxidative stress and inflammation.
Materials and methods: Forty-eight Wistar rats (230±20g) were divided into four groups. The control group comprised healthy animals, while the lesion group received Aβ1-40. The vehicle group received silibinin solvent post-Aβ1-40 injection. Treatment groups received silibinin (50, 100, and 200 mg/kg) after Aβ1-40 injection. Following a passive avoidance behavior test, biochemical analysis of superoxide dismutase, malondialdehyde, TNF-α, and IL-6 was conducted.
Results: Administration of 100 mg/kg silibinin significantly reduced serum IL-6 levels compared to the lesion group (P=0.005). All silibinin doses significantly decreased TNF-α levels (P≤0.001). Serum SOD levels increased significantly in animals treated with 100 and 200 mg/kg silibinin compared to the lesion group (P=0.002, P=0.03). Step-through latency improved in silibinin-treated animals (100 and 200 mg/kg) (P≤0.006).
Conclusions: These results suggest silibinin can enhance cognitive function and offer neuroprotection by inhibiting lipid peroxidation and reducing pro-inflammatory cytokines (TNF-α and IL-6) in AD rat models.

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Introduction: Evidence suggests that neuronal apoptosis in neurodegenerative diseases is correlated with inflammatory reactions. The beneficial or detrimental role of apoptosis in neuroinflammation is unclear. Elucidating this question may be helpful in management of neurodegenerative diseases. Since TNF-α is able to induce apoptosis as well as increased viability of the cells by activation of caspases or NF-kB, respectively, the question is what will happen if the balance between the two pathways is disturbed by inhibition of apoptosis. Methods: In this study, we used β–amyloid peptide (soluble Aβ monomer) injection into the Wistar male rat prefrontal cortex for induction of neuroinflammation in the hippocampus. Levels of TNF-α and caspase-3 were determined via western blot analysis. Using chronic intracerebroventricular administration of caspase inhibitors, z-VAD –fmk and z-DEVD-fmk, we inhibited apoptosis. Exploring consequences of apoptosis inhibition, activity of NF-kB was evaluated via western blotting. Results: After β–amyloid peptide injection we observed an increase in TNF-α and caspase3 as an inflammatory cytokine and apoptotic marker, respectively (P<0.001 and P<0.0001, respectively). As a consequences of apoptosis inhibition, nuclear NF-κB was decreased and cytosolic NF-κB was increased and these changes were significant compared to Aβ-injected group (P<0.001 and P<0.05, respectively). Conclusion: Caspase inhibition as an initiator of apoptosis, probably by attenuation of NF-kB activity, protect cells from abnormal survival and proliferation.

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Introduction: Tacca chantrieri Andre is frequently used by traditional healers to alleviate pain and fever, primirily by reducing inflammation. Its rhizome extract possesses remarkable peripheral anti-inflammatory and antioxidant bioactivities. However, there is limited information available regarding its potential anti-neuroinflammation effects. This study aimes to assess the neuroprotective effects of T. chantrieri rhizome ethanol extract (TCE) against lipopolysaccharides (LPS)-induced neuroinflammation.
Methods: Rats were orally administered with TCE at doses of 50, 100, and 200 mg/kg continually for 9 days. On the 7th day of treatment, each rat received a single intraperitoneal injection of LPS (0.83 mg/kg). Cognitive performance was assessed using the Y-maze test and novel object recognition (NOR) test. Thereafter, the proinflammatory cytokine level in the hippocampus was measured by ELISA.
Results: Systemic LPS administration induced sickness behavior, cognitive impairment, and neuroinflammation. TCE at doses of 100 and 200 mg/kg reversed the LPS-induced behavioral deficits, showing improvements in spontaneous alternation in the Y-maze test and discrimination index in the NOR test. Additionally, pretreatment with TCE at doses of 100 and 200 mg/kg significantly attenuated the LPS-induced increase in protein expression of TNF-α.
Conclusion: TCE exhibited neuroprotective effects against LPS-induced cognitive deficits and suppressed the production of pro-inflammatory mediators in a dose-dependent manner. These findings indicate that TCE may hold therapeutic potential in preventing neuroinflammation associated cognitive impairment. However, further studies are necessary to validate the possible mechanisms of its neuroprotective effects.