Purpose Cadmium (Cd), a potent neurotoxic heavy metal, elicits cerebral oxidative disturbances. Alginates are recognized for their chelating properties and their ability to bind with toxic agents and heavy metals. This study is designed to explore the neuroprotective potential of sodium alginate against cadmium chloride (CdCl2)-provoked noxious alterations in albino rats. Methods Thirty adult male Albino rats were randomly allocated into five groups, and each group had six animals (n = 6). Group I (control) rats received intraperitoneal (i.p.) injection of normal saline (10 ml/kg), Group II animals received 200 mg/kg, sodium alginate only, Group III animals were subjected to 5 mg/kg/day CdCl2, i.p., Group IV and V- rats received sodium alginate (100 mg/kg and 200 mg/kg; i.p.) per day respectively, along with CdCl2 (5 mg/kg) for 14 consecutive days. Spatial cognition was assessed using the Morris water maze. The cerebral oxidative injury (thiobarbituric acid reactive substances-TBARS, superoxide dismutase-SOD), neuronal inflammation (myeloperoxidase, interleukin-6, 10, and tumor necrosis factor-α), neurotransmitters (acetylcholinesterase, dopamine, and serotonin), and neurobiochemical markers (brain-derived neurotrophic factor-BDNF and cAMP response element-binding protein-CREB) were also assessed. The histological changes were also evaluated through H&E staining. Results CdCl2-treated rats exhibited symptoms such as cognitive deficits, along with disturbed antioxidant levels (raised TBARS and declined SOD), increased neuroinflammation, disrupted neurotransmitter levels, and decreased CREB and BDNF concentrations. Sodium alginate treatment alleviated the cognitive deficit and neuroinflammation in CdCl2-treated animals. It also restored the antioxidant level, cerebral function, neurotransmitters, and improved the histoarchitecture of the hippocampus of CdCl2-treated rats. Conclusion Findings of this study conclude that sodium alginate improved cognitive ability and exhibited anti-inflammatory and antioxidant properties. It also regulates neurotransmitters and neurotrophins in the brain; therefore, sodium alginate might have neuroprotective potential against CdCl2-provoked neurotoxic changes. Graphical Abstract

Sodium Alginate Offers Neuroprotection via Mitigating Inflammatory and Oxidative Markers in Cadmium-exposed Experimental Albino Rats

期刊论文
发表日期：

2026年5月19日

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Prince,
Surbhi Gupta,
Prabhat Singh,
Sachin Tyagi,
Bhupesh Sharma,
Vikram Singh

摘要

Purpose

Cadmium (Cd), a potent neurotoxic heavy metal, elicits cerebral oxidative disturbances. Alginates are recognized for their chelating properties and their ability to bind with toxic agents and heavy metals. This study is designed to explore the neuroprotective potential of sodium alginate against cadmium chloride (CdCl₂)-provoked noxious alterations in albino rats.

Methods

Thirty adult male Albino rats were randomly allocated into five groups, and each group had six animals (n = 6). Group I (control) rats received intraperitoneal (i.p.) injection of normal saline (10 ml/kg), Group II animals received 200 mg/kg, sodium alginate only, Group III animals were subjected to 5 mg/kg/day CdCl_2, i.p., Group IV and V- rats received sodium alginate (100 mg/kg and 200 mg/kg; i.p.) per day respectively, along with CdCl₂ (5 mg/kg) for 14 consecutive days. Spatial cognition was assessed using the Morris water maze. The cerebral oxidative injury (thiobarbituric acid reactive substances-TBARS, superoxide dismutase-SOD), neuronal inflammation (myeloperoxidase, interleukin-6, 10, and tumor necrosis factor-α), neurotransmitters (acetylcholinesterase, dopamine, and serotonin), and neurobiochemical markers (brain-derived neurotrophic factor-BDNF and cAMP response element-binding protein-CREB) were also assessed. The histological changes were also evaluated through H&E staining.

Results

CdCl₂-treated rats exhibited symptoms such as cognitive deficits, along with disturbed antioxidant levels (raised TBARS and declined SOD), increased neuroinflammation, disrupted neurotransmitter levels, and decreased CREB and BDNF concentrations. Sodium alginate treatment alleviated the cognitive deficit and neuroinflammation in CdCl₂-treated animals. It also restored the antioxidant level, cerebral function, neurotransmitters, and improved the histoarchitecture of the hippocampus of CdCl₂-treated rats.

Conclusion

Findings of this study conclude that sodium alginate improved cognitive ability and exhibited anti-inflammatory and antioxidant properties. It also regulates neurotransmitters and neurotrophins in the brain; therefore, sodium alginate might have neuroprotective potential against CdCl₂-provoked neurotoxic changes.

Graphical Abstract