Chia-Chih Liao

Background and Aims: Normal spontaneous delivery is often accompanied by various types of pain; postpartum uterine pain can persist for 2 or 3 days after childbirth. The quadratus lumborum block (QLB) is a relatively safe, cost‐effective, and efficacious pain management strategy used in various abdominal surgeries. The present study aimed to determine the effectiveness of QLB in relieving postpartum uterine contraction pain in the immediate 48 h postpartum period. Methods: Sixty‐six women, who normally and spontaneous delivered between May 2022 and August 2022, were randomly assigned to undergo either QLB with 0.375% ropivacaine or QLB with pure normal saline for postpartum uterine pain relief. Primary outcome was the severity/degree of uterine pain according to the visual analog scale (VAS) score. Pain interference impacting participants' activities of daily living before and 1, 6, 12, 24, 36, and 48 h after intervention was a secondary outcome. Results: Those in the ropivacaine group required significantly fewer rescue analgesics and exhibited substantially lower mean VAS pain scores at rest and during activity, and a lower level of pain interference when compared with those in the normal saline group ( p < 0.001) at 1, 6, 12, 24, 36, and 48 h after QLB. Conclusion: QLB was a valuable option for managing postpartum uterine pain after normal spontaneous delivery. It offered the benefits of stable hemodynamics, cost‐effectiveness, simplicity, and less pain interference with the activities of daily living, and minimal discomfort during the treatment process, with very few negative side effects. Trial Registration: study registered with the clinical trials registry website (12/05/2022). ClinicalTrials.gov identifier: NCT05371015.

Stachydrine, a major bioactive alkaloid extracted from Leonurus heterophyllus, is a key component of traditional herbal medicine, recognized for its anti-inflammatory and antioxidant properties. In this study, we investigated the gastroprotective effects of stachydrine and its underlying mechanisms in a mouse model of indomethacin (IND)-induced gastric injury. Mice were intragastrically administered IND at a dose of 40 mg/kg, followed 30 min later by treatment with varying doses of stachydrine (0, 5, and 10 mg/kg). Six hours post-IND administration, animals were sacrificed for further analysis. The results demonstrated that stachydrine treatment effectively attenuated IND-induced acute gastric injury, as evidenced by reduced gastric myeloperoxidase activity, and pro-inflammatory cytokine production (TNF-α, IL-6, and IL-1β). Stachydrine also significantly decreased gastric malondialdehyde activity while enhancing superoxide dismutase activity. Furthermore, it suppressed the expression of extracellular signal-regulated kinase (ERK), protein kinase B (AKT), and inducible nitric oxide synthase (iNOS) expressions. These findings indicate that stachydrine confers gastroprotection against IND-induced gastric injury, potentially by suppressing inflammatory and oxidative stress responses, inhibiting the ERK, AKT and iNOS signaling pathways. Thus, stachydrine may serve as a promising candidate for the treatment of IND-induced gastric injury.

Xanthoxylin, a bioactive phenolic compound extracted from the traditional herbal medicine Penthorum Chinense Pursh, is renowned for its anti-inflammatory effects. While previous studies have highlighted the anti-inflammatory and antioxidant properties of Xanthoxylin, its precise mechanisms, particularly concerning immune response and organ protection, remain underexplored. This study aimed to elucidate the effects of Xanthoxylin on inflammation and associated signaling pathways in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced via intratracheal administration of LPS, followed by intraperitoneal injections of Xanthoxylin at doses of 1, 2.5, 5, and 10 mg/kg, administered 30 min post-LPS exposure. Lung tissues were harvested for analysis 6 h after LPS challenge. Xanthoxylin treatment significantly mitigated lung tissue damage, pathological alterations, immune cell infiltration, and the production of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Additionally, Xanthoxylin modulated the expression of key proteins in the protein kinase B (Akt)/hypoxia-inducible factor 1-alpha (HIF-1α)/nuclear factor-kappa B (NF-κB) signaling pathway, as well as nuclear factor erythroid 2-related factor 2 (Nrf2) and oxidative markers such as superoxide dismutase (SOD) and malondialdehyde (MDA) in the context of LPS-induced injury. This study demonstrates that Xanthoxylin exerts protective and anti-inflammatory effects by down-regulating and inhibiting the Akt/HIF-1α/NF-κB pathways, suggesting its potential as a therapeutic target for the prevention and treatment of ALI or acute respiratory distress syndrome (ARDS).

Acute lung injury (ALI) and its severe manifestation, acute respiratory distress syndrome (ARDS), are characterized by uncontrolled inflammatory responses, neutrophil activation and infiltration, damage to the alveolar capillary membrane, and diffuse alveolar injury. Neutrophil extracellular traps (NETs), formed by activated neutrophils, contribute significantly to various inflammatory disorders and can lead to tissue damage and organ dysfunction. Corilagin, a compound found in Phyllanthus urinaria, possesses antioxidative and anti-inflammatory properties. In this study, we investigated the protective effects and underlying mechanisms of corilagin in hydrochloric acid (HCl)/lipopolysaccharide (LPS)-induced lung injury. Mice received intraperitoneal administration of corilagin (2.5, 5, or 10 mg/kg) or an equal volume of saline 30 min after intratracheal HCl/LPS administration. After 20 h, lung tissues were collected for analysis. Corilagin treatment significantly mitigated lung injury, as evidenced by reduced inflammatory cell infiltration, decreased production of proinflammatory cytokines, and alleviated oxidative stress. Furthermore, corilagin treatment suppressed neutrophil elastase expression, reduced NET formation, and inhibited the expression of ERK, p38, AKT, STAT3, and NOX2. Our findings suggest that corilagin inhibits NET formation and protects against HCl/LPS-induced ALI in mice by modulating the STAT3 and NOX2 signaling pathways.

Stachydrine, a prominent bioactive alkaloid derived from Leonurus heterophyllus, is a significant herb in traditional medicine. It has been noted for its anti-inflammatory and antioxidant characteristics. Consequently, we conducted a study of its hepatoprotective effect and the fundamental mechanisms involved in acetaminophen (APAP)-induced liver injury, utilizing a mouse model. Mice were intraperitoneally administered a hepatotoxic dose of APAP (300 mg/kg). Thirty minutes after APAP administration, mice were treated with different concentrations of stachydrine (0, 2.5, 5, and 10 mg/kg). Animals were sacrificed 16 h after APAP injection for serum and liver tissue assays. APAP overdose significantly elevated the serum alanine transferase levels, hepatic pro-inflammatory cytokines, malondialdehyde activity, phospho-extracellular signal-regulated kinase (ERK), phospho-protein kinase B (AKT), and macrophage-stimulating protein expression. Stachydrine treatment significantly decreased these parameters in mice with APAP-induced liver damage. Our results suggest that stachydrine may be a promising beneficial target in the prevention of APAP-induced liver damage through attenuation of the inflammatory response, inhibition of the ERK and AKT pathways, and expression of macrophage-stimulating proteins.

Recent experimental studies have highlighted the beneficial effects of curcumin on liver injury induced by acetaminophen (APAP). However, the specific molecular mechanisms underlying curcumin’s hepatoprotective effects against APAP-induced liver injury remain to be fully elucidated. This study aimed to investigate the therapeutic effect of curcumin on APAP-induced liver injury using a mouse model. In the experiment, mice were subjected to an intraperitoneal hepatotoxic dose of APAP (300 mg/kg) to induce hepatotoxicity. After 30 min of APAP administration, the mice were treated with different concentrations of curcumin (0, 10, 25, or 50 mg/kg). After 16 h, mice with hepatotoxicity showed elevated levels of serum alanine transaminase (ALT), aspartate transaminase (AST), hepatic myeloperoxidase (MPO), TNF-α, and IL-6, and decreased levels of glutathione (GSH). Moreover, there was an increased infiltration of neutrophils and macrophages following intraperitoneal injection of APAP. However, curcumin-treated mice displayed a pronounced reduction in serum ALT, AST, hepatic MPO, TNF-α, and IL-6 levels, coupled with a notable elevation in GSH levels compared to the APAP-treated hepatotoxic mice. Moreover, curcumin treatment led to reduced infiltration of neutrophils and macrophages. Additionally, curcumin inhibited the phosphorylation of ERK and NF-kB proteins while reducing the expression of cyclooxygenase-2 (COX-2). These findings highlight the hepatoprotective potential of curcumin against APAP-induced liver injury through the suppression of the ERK, NF-kB, and COX-2 signaling pathways.

Epidural anesthesia (EA) is the regional anesthesia technique preferred over spinal anesthesia for pregnant women requiring cesarean section and post-operative pain control. EA failure requires additional sedation or conversion to general anesthesia (GA). This may be hazardous during sedation or GA conversion because of potentially difficult airways. Therefore, this retrospective study aimed to determine the risk factors for epidural failure during cesarean section anesthesia. We retrospectively analyzed parturients who underwent cesarean section under EA and catheterization at the Chang Gung Memorial Hospital in Taiwan between January 1 and December 31, 2018. Patient data were collected from the medical records. EA failure was defined as the administration of any intravenous anesthetic at any time during a cesarean section, converting it into GA. A total of 534 parturients who underwent cesarean section were recruited for this study. Of them, 94 (17.6%) experienced EA failure during cesarean section. Compared to the patients with successful EA, those with EA failure were younger (33.0 years vs. 34.7 years), had received EA previously (60.6% vs. 37%), were parous (72.3% vs. 55%), and had a shorter waiting time (14.9 min vs. 16.5 min) (p < 0.05). Younger age (OR 0.91, 95% CI 0.86–0.95), history of epidural analgesia (OR 2.61, 95% CI 1.38–4.94), and shorter waiting time (OR 0.91, 95% CI 0.87–0.97) were estimated to be significantly associated with a higher risk of epidural anesthesia failure. The retrospective study found that parturients of younger age, previous epidural catheterization history, and inadequate waiting time may have a higher risk of EA failure. Previous epidural catheterization increased the risk of EA failure by 2.6-fold compared to patient with no history of catheterization.

Background: Epidural anesthesia (EA) is the preferred regional anesthesia technique in pregnant women who require cesarean section for delivery. Failure of EA requires additional sedation or convert it into general anesthesia (GA). It may be hazardous during sedation or GA conversion due to a potentially difficult airway. Therefore, this retrospective study aimed to determine the risk factors for epidural failure during cesarean section anesthesia. Methods: We retrospectively analyzed parturients who underwent cesarean section under EA and catheterization at Chang Gung Memorial Hospital in Taiwan between January 1 and December 31, 2018. Patient data were collected from medical records. EA failure was defined as the administration of any intravenous anesthetic at any time during the cesarean section, converting it into GA or even tube GA. Results: A total of 534 parturients who underwent cesarean section were recruited for this study. Of these, 94 (17.6%) parturients experienced failure of EA during the cesarean section. Compared to the patients with successful EA, those with EA failure were younger (33.0 years vs. 34.7 years) and have received EA previously (60.6% vs. 37%), were parous (72.3% vs. 55%), and had a shorter waiting time (14.9 mins vs. 16.5 mins) (p < 0.05). Younger age (OR 0.91, 95% CI 0.86–0.95), history of epidural analgesia (OR 2.61, 95% CI 1.38–4.94), and shorter waiting time (OR 0.91, 95% CI 0.87–0.97) were estimated to be significantly associated with a higher risk of epidural anesthesia failure. Conclusion: The retrospective study found that parturients with younger age, previous epidural catheterization history, and inadequate waiting time may have a higher risk of EA failure. Previous epidural catheterization increases the risk of EA failure by 2.6-folds compared to those with no catheterization history.

Acetaminophen (APAP) overdose causes acute liver injury via oxidative stress, uncontrolled inflammatory response, and subsequent hepatocyte death. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a potent source of cellular reactive oxygen species (ROS) and may contribute to oxidative stress in many inflammatory processes. Corilagin, a component of Phyllanthus urinaria, possesses antioxidant, anti-inflammatory, and hepatoprotective effects. We evaluated the mechanisms underlying the protective effect of corilagin against acetaminophen-induced liver injury. Mice were intraperitoneally administrated 300 mg/kg APAP or equal volume of saline (control), with or without various concentrations of corilagin (0, 1, 5, or 10 mg/kg) administered after 30 min. All animals were sacrificed 16 h after APAP administration, and serum and liver tissue assays including histology, immunohistochemistry, and Western blot assay were performed. Corilagin post-treatment significantly attenuated APAP-induced liver injury (p < 0.005), inflammatory cell infiltration, hepatic proinflammatory cytokine levels, and hepatic oxidative stress. Furthermore, corilagin attenuated the protein levels of NOX1, NOX2, signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa B (NF-κB) in APAP-induced liver injury. These results indicated that the antioxidant, anti-inflammatory, and protective effects of corilagin in APAP-induced liver injury might involve the regulation of interleukin (IL)-6/STAT3 and mitogen-activated protein kinase (MAPK)/NF-κB signaling pathways through NOX-derived ROS.