## 4 Discussion
This restoration of phase II enzymes by _Carum carvi_ was also supported by [34]. It has been depicted that, in acetaminophen-induced liver toxicity, apoptosis (programmed cell death) plays a significant role [35]. Thus, for the prevention of acetaminophen-induced liver toxicity, interventions to prevent apoptosis can serve as one of the promising tools. In this study, evaluation of effector caspase (3 and 7) and initiator caspase (caspase 9) activities was carried out in acetaminophen-induced liver toxicity in rats. Fodrin, poly (ADP-ribose) polymerase (PARP), and nuclear lamin proteins are degraded or cleaved by effector caspases 3 and 7; therefore, these caspases are considered to be among the key executioners of apoptosis. An attempt was made to determine if _Carum carvi_ extract could reduce DNA damage and apoptosis in the liver of acetaminophen-treated rats. The decline in caspase activity by _Carum carvi_ action indicates the mechanism via which _Carum carvi_ alleviated acetaminophen-induced apoptosis and toxicity. Oxidative stress promotes the activation of proinflammatory genes, which eventually stimulate inflammatory cells to overproduce ROS. This vicious cycle leads to the onset and progression of numerous diseases. As a result, the liver's detoxification system is crucial when the body is exposed to toxic substances, and the inflammatory process can exacerbate tissue damage and result in poor healing [36]. There is growing confirmation that paracetamol intoxication can raise several proinflammatory cytokine levels in the blood. Oxidative stress activates signal transduction pathways involving NF-kB and activator protein-1 (AP-1) [37]. A vital signaling pathway is NF-kB, which facilitates the synthesis of molecules associated with inflammation, such as by incorporating NF-kB-binding motifs in their promoters. When paracetamol is administered, the NF-kB protein is activated, which increases the activity of iNOS, TNF-\(\alpha\), and COX-2 [38]. Inflammation plays a crucial role in acetaminophen overdose-induced liver toxicity, which is mediated by the activation of transcription factor NF-kB and the secretion of several cytokines such as TNF-\(\alpha\) and IL-1\(\beta\). Activated NF-kB is then translocated into the nucleus, resulting in the induction of chemokines and proinflammatory enzymes, including iNOS and COX-2. It has been reported that acetaminophen overdose leads to an inflammatory reaction and oxidative stress, resulting in the production of iNOS and reactive nitrogen species. Both iNOS and COX-2 exert their activities in a similar way by inducing inflammatory response [39]. Furthermore, iNOS expression causes an excessive amount of NO to be produced, which heightens the immune response by triggering inflammatory cell signaling transduction. Therefore, it is assumed that decreasing NO levels by blocking iNOS expression is a desirable first step in assessing the effectiveness of novel drugs in the management of inflammatory conditions [40]. Our results completely coincide with those reported by [PERSON] et al., whereby acetaminophen administration to rats resulted in higher expressions on NF-kB and TNF-\(\alpha\). _Carum carvi_ exhibited potential efficacy in alleviating acetaminopheninduced expression of NF-kB and TNF-\(\alpha\). The anti-inflammatory properties of _Carum carvi_ have been reported by researchers in experiments including colitis [41]. Similar findings of anti-inflammatory properties have been reported by various research studies [42; 43; 44]. Moreover, studies have confirmed that _Carum carvi_ possesses effects in wound healing, liver protection, antioxidant, pain management, antifungal, and diuretic properties [42; 44; 45; 46]. Therefore, the findings postulate that _Carum carvi_ could prove to be a vital molecule to suppress the drug-mediated hepatotoxicity by protecting liver cells; however, further studies are needed.