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Gene & Protein in Disease Modulating immune response in liver by curcumin

thereby providing protection against these harmful guanidine, glutamic oxaloacetic transaminase, glutamate
processes. In vitro studies conducted on murine models pyruvate transaminase, and lactate dehydrogenase. These
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have demonstrated the advantageous effects of curcumin findings suggest that curcumin has the potential to mitigate
in preventing liver injury caused by various factors. 73,74 exacerbated inflammation and oxidative stress responses
It is hypothesized that curcumin’s interaction with heme during reperfusion liver injury.
oxygenase-1 (HO-1), a crucial mediator of cytoprotective On a broader scale, drug-induced liver toxicity is a
events, may offer a plausible explanation for its mode of significant concern, with numerous drugs capable of causing
action. The hepatoprotective properties of curcumin adverse effects on the liver. Drugs used for anti-cancer, anti-
have been proven in a study using rat models, where a analgesic, anti-inflammatory, and antidepressant purposes
single intraperitoneal dose of curcumin at 100 mg/kg was are particularly associated with hepatotoxic properties.
associated with the upregulation of HO-1 and subsequent The underlying mechanisms of drug-induced liver damage
production of bilirubin. This effect was accompanied involve ROS, reactive nitrogen species, mitochondrial
by the downregulation of NO synthase 2 (NOS-2) and dysfunction, and lipid dysmetabolism. Paracetamol, a
NO, which controlled lipid peroxidation. A similar study commonly used antipyretic, is often responsible for drug-
revealed that prophylactic administration of curcumin at induced liver damage. However, studies have shown that
a dose of 300 mg/kg/day orally for seven days exhibited curcumin, a natural compound known for its antioxidant
chemopreventive capacity against micro cystins-induced and anti-inflammatory properties, can effectively mitigate
liver injury, as indicated by a statistically significant paracetamol-induced hepatotoxicity. In experiments
reduction in liver-specific enzyme levels compared to conducted on rabbits, supplementation with curcumin at
a group treated with micro cystins alone. The study also doses of 50 and 100 mg/kg/day resulted in a decrease in
found positive changes in malondialdehyde (MDA) levels elevated levels of AST, ALP, and ALT, while simultaneously
and negative changes in superoxide dismutase (SOD) increasing total protein and albumin levels in plasma.
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levels, indicating that curcumin can enhance the liver’s Beyond its protective effects against paracetamol-induced
antioxidative abilities in mice. Similarly, in Wistar albino liver damage, curcumin has also demonstrated efficacy in
rats, a similar reduction in oxidative stress and DNA addressing hepatotoxicity caused by other substances. For
damage was observed after 14 days of oral curcumin example, in a rat model of hepatotoxicity induced using
administration, suggesting that curcumin improves liver propanil, a herbicide used for weed control, curcumin
function, particularly in protecting against damages demonstrated its ability to alleviate the effects of propanil
caused by cholestasis. Furthermore, histopathological
evaluation showed that curcumin decreased ductal intoxication by reducing lipid peroxidation levels, restoring
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proliferation and portal inflammation compared to the serum enzyme levels, and enhancing reduced glutathione.
induced group, indicating a significant reduction in the Curcumin’s hepatoprotective properties have been
inflammatory process. Similarly, curcumin facilitated a observed in cases of liver damage induced by thioacetamide
statistically significant reduction in MDA, glutathione, (TAA). TAA is known to increase levels of ROS and
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NO, and TNF-α levels, while enhancing catalase, SOD, activate HSCs, both of which contribute to liver injury. In
and glutathione S-transferase activities in the liver a rat model of TAA-induced hepatotoxicity, curcumin was
following biliary duct ligation (BDL)-induced liver found to reduce oxidative stress and suppress the expression
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injury. Curcumin’s ability to protect against BDL-induced of the angiotensin-converting enzyme gene. These
hepatic damage through antioxidant action was further effects led to the protection of liver tissue, restoration of
demonstrated in another study conducted on Wistar antioxidant enzyme levels, and preservation of hepatocytes.
rat liver tissue. The study reported downregulation of Furthermore, studies have shown that curcumin can
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NADPH oxidase-1, Rac1-guanosine triphosphate, and mitigate acute TAA hepatotoxicity by decreasing levels of
Rho-related C3 botulinum toxin substrate, along with thiobarbituric acid reactive substances, reducing oxidative
increased hepatic enzyme levels (e.g., alkaline phosphatase stress, and inhibiting the production of inducible NOS and
[ALP], aspartate transaminase [AST], alanine transaminase NF-κB. These findings highlight curcumin’s potential in
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[ALT]) and protective agents (e.g., thiols, catalase, SOD). alleviating the extensive damage caused by TAA in the
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In female Wistar albino rats, pretreatment with curcumin liver. In addition, curcumin has been investigated for its
at a dose of 100 mg/kg administered intraperitoneally protective effects in cases of hepatotoxicity induced by
30 minutes before ischemia/reperfusion was found to have LPS, nanoparticles, and sodium fluoride. LPS-induced
a hepatoprotective effect against liver injury. This hepatic hepatotoxicity is characterized by increased production
protective effect was evidenced by a reduction in liver of reactive oxygen intermediates, lipid peroxidation,
injury markers in the blood, such as NO, TNF-α, methyl migration of activated polymorphonuclear neutrophils

Volume 3 Issue 3 (2024) 10 doi: 10.36922/gpd.3186