Neuroprotective effects of Hibiscus sabdariffa var. altissima on cerebral ischemia‒Reperfusion injury in rats

• Published in: Pharmacological research. Modern Chinese medicine Vol. 12; p. 100485
• Main Authors: Hamadjida, Adjia, Njemguie, Saida Nkuketgnigni, Mbomo, Rigobert Espoir Ayissi, Foudjih, Stephen Nkengbang, Amayapa, Véronique France Prisca, Mingoas, Jean Pierre Kilekoung, Ntchapda, Fidèle
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01-09-2024; Elsevier
• Subjects: Cerebral ischemia; Hibiscus sabdariffa var. altissima; Inflammation; Mcao; Neuroprotective; Oxidative stress; Mcao; Neuroprotective; Oxidative stress; Cerebral ischemia; Inflammation; Hibiscus sabdariffa var. altissima
• ISSN: 2667-1425; 2667-1425
• DOI: 10.1016/j.prmcm.2024.100485

•In the ischemic rats, Hibiscus sabdariffa var. altissima improves neurological function.•In the ischemic rats, Hibiscus sabdariffa var. altissima reduces cerebral infraction.•In the ischemic rats, Hibiscus sabdariffa var. altissima inhibits oxidative stress.•In the ischemic rats, Hibiscus sabdariffa var. altissima attenuates inflammation.•Thus, Hibiscus sabdariffa var. altissima protects against ischemic-reperfusion injury.
Hibiscus sabdariffa var. altissima, which is known for its high-quality fiber, is commonly used in Traditional Chinese Medicine (TCM) for its diuretic, choleretic, analgesic, antitussive, and hypotensive effects. Furthermore, the flowers have been used to treat diabetes, hypertension, atherosclerosis, and obesity. However, there are no studies assessing its neuroprotective effects on cerebral ischemia, unlike the sabdariffa variety known for its neuroprotective effects. Therefore, this study was aimed to investigate the potential efficacy of Hibiscus sabdariffa var. altissima extract (HAS) and its underlying mechanism on oxidative stress and neuroinflammation during cerebral ischemia-reperfusion (I/R) injury.
A model of cerebral ischemia was established in male Wistar rats through middle cerebral artery occlusion (MCAO) and reperfusion. Rats were randomly divided into the sham, IR, IR + HSA100, IR + HSA200, IR + HSA400 and IR + Eda groups and were treated for 14 consecutive days. The neurological deficit score and the cylinder test were performed to assess neurological impairment. Oxidative stress was determined by measuring the levels of malondialdehyde (MDA) and antioxidant markers such as reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were measured to evaluate antioxidant activities. In addition, the levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), were also determined.
Our results demonstrated that HSA significantly ameliorated neurological impairment and reduced the volume of brain infarct. HSA also decreased the levels of MDA and enhanced the antioxidant activities of GSH, SOD and CAT in brain tissues. Furthermore, HSA decreased the expression of the proinflammatory cytokines TNF-α, IL-1β and IL-6 in the serum.
These findings demonstrated that HSA exhibited a potential neuroprotective effect against cerebral I/R injury, possibly by improving oxidative stress and attenuating inflammatory responses. Therefore, HSA could be used as a potential therapeutic option for cerebral ischemic injuries.
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