{"id":54656,"date":"2023-12-31T10:44:07","date_gmt":"2023-12-31T10:44:07","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=54656"},"modified":"2024-01-18T08:34:46","modified_gmt":"2024-01-18T08:34:46","slug":"protective-effect-of-aspirin-against-gentamicin-induced-hepatotoxicity-in-rats-model","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol16no4\/protective-effect-of-aspirin-against-gentamicin-induced-hepatotoxicity-in-rats-model\/","title":{"rendered":"Protective Effect of Aspirin Against Gentamicin-Induced Hepatotoxicity in Rats Model"},"content":{"rendered":"\n

Introduction<\/strong><\/p>\n\n\n\n

The use of certain medications, while\nbeneficial for treating various conditions, can sometimes lead to adverse\neffects on the liver. Gentamicin, a widely used antibiotic, has been associated\nwith hepatotoxicity, which refers to liver damage caused by toxic substances.\nIn recent years, research has focused on exploring potential protective agents\nthat can mitigate the hepatotoxic effects of gentamicin. One such agent of\ninterest is aspirin, a commonly used medication with known anti-inflammatory\nand antioxidant properties1<\/sup>.<\/p>\n\n\n\n

Gentamicin-induced hepatotoxicity is\ncharacterized by liver dysfunction, increased liver weight, and an increase in liver\nenzymes, including alanine aminotransferase (ALT) and aspartate\naminotransferase (AST), in the serum. Hepatic lipid peroxidation, reduction in\nthe level of antioxidants, and impairment of cellular functions contribute to\nthe development of gentamicin-induced liver injury. Aspirin, also known as\nacetylsalicylic acid, has been investigated for its potential hepatoprotective\nproperties. Studies have suggested that aspirin possesses antioxidant and\nanti-inflammatory properties, which may help alleviate liver damage induced by\ngentamicin2-4<\/sup>. The mechanism underlying the protective effect of\naspirin is believed to involve the inhibition of oxidative stress and the\nmodulation of inflammatory pathways.<\/p>\n\n\n\n

The goal of this study was to examine the effect\nof aspirin on gentamicin-induced hepatotoxicity in an animal model.\nSpecifically, we examined the impact of aspirin on liver weight, serum liver\nenzymes (ALT and AST), as well as oxidative stress markers, such as malondialdehyde\n(MDA), glutathione (GSH), nitric oxide (NO), and catalase activity. Male Wistar\nrats were randomly grouped into four: control, aspirin group, gentamicin group,\nand aspirin-gentamicin group5<\/sup>. The animals were treated according to\nthe designated groups, and liver weight, serum liver enzymes, and oxidative\nstress markers were assessed during the experimental time. The doses of\ngentamicin and aspirin were chosen to depend on previous studies6-7<\/sup>.<\/p>\n\n\n\n

Material and Method<\/strong><\/p>\n\n\n\n

Drugs<\/strong><\/p>\n\n\n\n

Gentamicin (CAS- No 1405410, 100 pure) and aspirin (CAS- No 502658 chastity 98) were purchased from Sigma- Aldrich Chemical Company (St.Louis, Missouri, USA). Other reagents were of logical grade.<\/p>\n\n\n\n

Animals<\/strong><\/p>\n\n\n\n

Wistar rats (70 \u2013 80 days old) importing were selected (Faculty of Pharmacy, King Faisal University,), housed in clean polypropylene coops, and maintained on a 12- hour light\/ dark cycle at a temperature of 20 \u2013 25C with ad libitum access to standard food and water.7 days pre-experimental rats were handled daily for minimize their physiological responses to handling for posterior protocols. All treatment described was performed according to the Research Ethics Committee of King Faisal University.<\/p>\n\n\n\n

Experimental protocol<\/strong><\/p>\n\n\n\n

Animals were sectioned into four groups consisting of six rats each. Group I(control) entered the vehicle. Group II (aspirin group) entered aspirin 10mg\/ ml (200mg\/ kg\/ day intragastrical). Group III (gentamicin group) was treated with gentamicin (100 mg\/ kg\/ day by intraperitoneal) in a single injection. Group IV (aspirin- gentamicin group) was treated with aspirin and gentamicin by the same schedule. Groups II and IV entered aspirin from day 1 until day 15(the total period of the trial). Groups III and IV entered gentamicin for 10 successive days, starting from the sixth day of the trial until day 15. The selected doses of gentamicin and aspirin were chosen based on previous studies7<\/sup>. <\/p>\n\n\n\n

Sample medication and biochemical tests<\/strong><\/p>\n\n\n\n

animals were killed by stunning and cervical dislocation under Schedule 1 according to the United Kingdom Animals (Scientific Procedures) Act 1986 a day after the last dose of gentamicin. blood samples were taken and left for 1 hour to clot. Centrifuge blood sample for 10 twinkles at 5000 rpm to get a pure serum that was also stored at a 20-degree temperature. To estimate serum aspartate aminotransferase as well as alanine aminotransferase kit (Randox Laboratories Ltd. UK, recommending, colorimetric accouterments) were used.<\/p>\n\n\n\n

liver tissue washed with ice-cold saline and stored at 80-degree temperature. exercising cold potassium phosphate buffer, the liver was homogenized. Homogenates were separated at 5000 rpm for 10 twinkles at 4 \u2103 and the supernatant was used for determining malondialdehyde and minimizing glutathione degree and exertion of catalase exercising colorimetric accoutrements of the assay as framed by the manufacturer’s instructions forbio-diagnostic (Bodaghi- Namilehet.al. 2018). Depending on the manufacturer, Cayman Chemical Co, USA, instructions, the degree of nitric oxide (NO) level was determined by exercising a tackle of the colorimetric assay.<\/p>\n\n\n\n

Statistical analysis<\/strong><\/p>\n\n\n\n

To assay the collected data, all the data were expressed as mean \u00b1S.E.M (pars of the repeated trials). A one-way analysis of friction (ANOVA) was done, followed by the Tukey test for the multiple comparisons. SPSS interpretation 21 was used. The differences were determined at the significance position of p<0.05.<\/p>\n\n\n\n

Results<\/strong><\/p>\n\n\n\n

Effects of aspirin on the measured biochemical parameters<\/strong><\/p>\n\n\n\n

Treatment rats with gentamicin significantly increased liver weight compared to control rats (figure 1) whereases treatment rats with aspirin were suitable to reverse the effect of gentamicin on liver weight. While in Figure 2, dramatic increase in serum alanine aminotransferase and aspartate aminotransferase situations was witnessed in the animals that were subjected to gentamicin compared to the control group. Our results demonstrated that the treatment of aspirin, after gentamicin administration urged a significant reduction in the serum situations of the aminotransferases. Further, the treatment with aspirin significantly suppressed hepatic lipid peroxidation and averted reductions in GSH position and catalase exertion because of gentamicin administration.<\/p>\n\n\n\n\n\n
\"\"<\/td>\nFigure 1: Effect of aspirin on liver weight variation of gentamicin-induced hepatotoxicity\u00a0in rats. <\/strong>\n

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Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u00a0<\/p>\n\n\n\n
\"\"<\/td>\nFigure 2: Factors Influencing the Knowledge, Attitude and Use of CAM Modalities.<\/strong>\n

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Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

Table 1: Effect of aspirin on antioxidant levels in gentamicin-induced hepatotoxicity in animals. All the values are expressed as mean \u00b1 S.E.M., n = 8 in each group. a<\/sup> p < 0.05 vs. control group.b<\/sup> p < 0.05 vs. gentamicin.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n
\n

GSH (mg\/g tissue)<\/strong><\/p>\n<\/td>\n

\n

NO (nmol\/100mg tissue)<\/strong><\/p>\n<\/td>\n

\n

MDA<\/strong><\/p>\n<\/td>\n

\n

CATALASE (u\/g tissue)<\/strong><\/p>\n<\/td>\n

\n

Dose (mg\/kg)<\/strong><\/p>\n<\/td>\n

\n

Treatment<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

115.3\u00b11.2<\/p>\n<\/td>\n

\n

90.3\u00b10.6<\/p>\n<\/td>\n

\n

25.50\u00b10.36<\/p>\n<\/td>\n

\n

5.5\u00b10.47<\/p>\n<\/td>\n

 <\/td>\n\n

Control<\/p>\n<\/td>\n<\/tr>\n

\n

105\u00b14.3 a<\/sup><\/p>\n<\/td>\n

\n

102.3\u00b11.55 a<\/sup><\/p>\n<\/td>\n

\n

51.71\u00b11.03 a<\/sup><\/p>\n<\/td>\n

\n

3.4\u00b10.32 a<\/sup><\/p>\n<\/td>\n

\n

100mg\/kg<\/p>\n<\/td>\n

\n

gentamicin<\/p>\n<\/td>\n<\/tr>\n

\n

134.4\u00b13.3<\/p>\n<\/td>\n

\n

132.7\u00b11.3<\/p>\n<\/td>\n

\n

36.8\u00b10.47<\/p>\n<\/td>\n

\n

4.7\u00b10.56<\/p>\n<\/td>\n

\n

200mg\/kg<\/p>\n<\/td>\n

\n

aspirin<\/p>\n<\/td>\n<\/tr>\n

\n

116.4\u00b11.8 b<\/sup><\/p>\n<\/td>\n

\n

109.7\u00b11.02 b<\/sup><\/p>\n<\/td>\n

\n

40.26\u00b10.82 b<\/sup><\/p>\n<\/td>\n

\n

5.3\u00b10.54 b<\/sup><\/p>\n<\/td>\n

\n

 <\/p>\n<\/td>\n

\n

Aspirin+ gentamicin<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

*MDA: malondialdehyde, NO: nitric oxide, GSH: glutathione.<\/p>\n\n\n

Discussion<\/strong><\/p>\n\n\n\n

The current study aimed to examine the effect\nof aspirin against gentamicin-induced hepatotoxicity in a rat model. The\nresults demonstrated that pre-treatment with aspirin significantly mitigated\nthe adverse effects of gentamicin on liver weight, serum liver enzymes, and\noxidative stress markers.<\/p>\n\n\n\n

Gentamicin administration resulted in a dramatically\nelevation in liver weight, which is indicative of liver damage. This elevated liver\nweight may be caused by edema, congestion, and cellular infiltration caused by\nthe toxic effects of gentamicin on hepatocytes8<\/sup>. However,\npre-treatment with aspirin reversed this effect, suggesting a protective role\nagainst gentamicin-induced hepatotoxicity 9-11<\/sup>. The ability of\naspirin to counteract the increase in liver weight may be attributed to its\nanti-inflammatory properties, as inflammation is known to contribute to liver\ninjury. Aspirin’s anti-inflammatory effects have been well documented and may\ninvolve the inhibition of pro-inflammatory cytokines, such as tumor necrosis\nfactor-alpha (TNF-\u03b1) and interleukin-6 (IL-6), and the modulation of various\nsignaling pathways involved in the inflammatory response 12<\/sup>.<\/p>\n\n\n\n

Elevation in liver enzymes is usually known\nas the prediction of hepatocellular damage. In this study, gentamicin\nadministration led to a significant elevation in serum ALT and AST levels,\nindicating liver injury 13<\/sup>. However, pre-treatment with aspirin\nsignificantly reduced the serum levels of these liver enzymes. This finding\nsuggests that aspirin exerted a protective effect on liver cells and preserved their\nstructural and functional integrity 14-16<\/sup>. The mechanisms underlying\nthe hepatoprotective effects of aspirin may involve the inhibition of\ninflammation-induced hepatocyte apoptosis and the modulation of oxidative\nstress pathways 17<\/sup>. Aspirin has been shown to inhibit the release of\npro-inflammatory mediators and to promote the expression of anti-apoptotic\nproteins, thereby preventing hepatocyte damage and promoting cell survival.<\/p>\n\n\n\n

Oxidative stress plays a crucial role in\ngentamicin-induced hepatotoxicity. Increased release of reactive oxygen species\n(ROS) and impaired antioxidant defense mechanisms contribute to liver cell\ndamage 18<\/sup>. In the present study, aspirin treatment significantly\nsuppressed hepatic lipid peroxidation, as evidenced by the reduction in\nmalondialdehyde (MDA) levels 16<\/sup>. This indicates that aspirin acted\nas an antioxidant and attenuated lipid peroxidation, thereby protecting liver\ncells from oxidative damage. Aspirin’s antioxidant properties may be attributed\nto its capability to kick free radicals out of the body, inhibit ROS\nproduction, and enhance the activity of endogenous antioxidant enzymes 18-22<\/sup>.<\/p>\n\n\n\n

Moreover, aspirin treatment reduced the\ndepletion of glutathione (GSH) levels and catalase activity induced by\ngentamicin application. GSH is an important endogenous antioxidant that helps\nneutralize ROS and maintain redox balance in cells 14-19<\/sup>. Catalase\nis an enzyme involved in the detoxification of hydrogen peroxide, a reactive\noxygen species. The preservation of GSH levels and catalase activity by aspirin\nsuggests its ability to enhance the antioxidant defense mechanisms in the liver\nand protect against oxidative stress-induced liver injury14-20<\/sup>.\nAspirin may exert its effects on GSH and catalase through the modulation of\ntranscription factors and signaling pathways involved in antioxidant gene\nexpression and activity.<\/p>\n\n\n\n

The mechanism underlying the protective\neffect of aspirin against gentamicin-induced hepatotoxicity is likely\nmultifactorial. Aspirin possesses anti-inflammatory properties, which can\nattenuate inflammation-induced liver injury. It also acts as an antioxidant,\nreducing oxidative stress and preventing oxidative damage to liver cells.\nAdditionally, aspirin may modulate signaling pathways involved in cell survival\nand apoptosis, contributing to its hepatoprotective effects.<\/p>\n\n\n\n

The findings of this study support previous research indicating the potential hepatoprotective properties of aspirin. However, further investigations are warranted to elucidate the exact molecular mechanisms underlying its protective effects and to determine the optimal dosage and duration of aspirin treatment for maximum efficacy. Additionally, future studies should explore the long-term effects of aspirin treatment, as well as its potential interactions with other medications commonly co-administered with gentamicin15<\/sup>.<\/p>\n\n\n\n

Conclusion<\/strong><\/p>\n\n\n\n

In conclusion, this study demonstrates that\npre-treatment with aspirin attenuates gentamicin-induced hepatotoxicity in a\nrat model. Aspirin mitigated liver damage, preserved liver function, and\nenhanced antioxidant defense mechanisms. These findings highlight the potential\nof aspirin as a protective agent against drug-induced liver injury. Further\nstudies are needed to fully understand the mechanisms involved and to explore\nits clinical applications in humans. The use of animal models provides valuable\ninsights into the potential benefits of aspirin in the prevention and\nmanagement of hepatotoxicity, but further clinical trials are necessary,\nespecially in high-risk patients treated with gentamicin to establish its\nefficacy and safety in human patients13<\/sup>.<\/p>\n\n\n\n

To conclude,\nthe findings of this work provide evidence for the protective effect of aspirin\nagainst gentamicin-induced hepatotoxicity in a rat model. Pre-treatment with aspirin\ndemonstrated beneficial effects on liver weight, serum liver enzymes, and\noxidative stress markers. These findings suggest that aspirin possesses\nhepatoprotective properties and may be a potential therapeutic option for the\nprevention and management of drug-induced liver injury.<\/p>\n\n\n\n

Acknowledgment<\/strong><\/p>\n\n\n\n

Thanks to deanship of scientific research king faisal university for supporting this work  (grant 5181).<\/p>\n\n\n\n

Conflict of Interest<\/strong> <\/p>\n\n\n\n

The authors declare no conflict of interest. <\/p>\n\n\n\n

Funding source<\/strong><\/p>\n\n\n\n

There is no funding source.<\/p>\n\n\n\n

References<\/strong><\/p>\n\n\n\n

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