Huangqin decoction alleviates lipid metabolism disorders and insulin resistance in nonalcoholic fatty liver disease by triggering Sirt1/NF-κB pathway.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a clinicopathological entity characterized by intrahepatic ectopic steatosis. As a consequence of increased consumption of high-calorie diet and adoption of a sedentary lifestyle, the incidence of NAFLD has surpassed that of viral hepatitis, making it the most common cause of chronic liver disease globally. Huangqin decoction (HQD), a Chinese medicinal formulation that has been used clinically for thousands of years, has beneficial outcomes in patients with liver diseases, including NAFLD. However, the role and mechanism of action of HQD in lipid metabolism disorders and insulin resistance in NAFLD remain poorly understood. AIM: To evaluate the ameliorative effects of HQD in NAFLD, with a focus on lipid metabolism and insulin resistance, and to elucidate the underlying mechanism of action. METHODS: High-fat diet-induced NAFLD rats and palmitic acid (PA)-stimulated HepG2 cells were used to investigate the effects of HQD and identify its potential mechanism of action. Phytochemicals in HQD were analyzed by high-performance liquid chromatography (HPLC) to identify the key components. RESULTS: Ten primary chemical components of HQD were identified by HPLC analysis. In vivo, HQD effectively prevented rats from gaining body and liver weight, improved the liver index, ameliorated hepatic histological aberrations, decreased transaminase and lipid profile disorders, and reduced the levels of pro-inflammatory factors and insulin resistance. In vitro studies revealed that HQD effectively alleviated PA-induced lipid accumulation, inflammation, and insulin resistance in HepG2 cells. In-depth investigation revealed that HQD triggers Sirt1/NF-κB pathway-modulated lipogenesis and inflammation, contributing to its beneficial actions, which was further corroborated by the addition of the Sirt1 antagonist EX-527 that compromised the favorable effects of HQD. CONCLUSION: In summary, our study confirmed that HQD mitigates lipid metabolism disorders and insulin resistance in NAFLD by triggering the Sirt1/NF-κB pathway.

Lithium promotes recovery after spinal cord injury.

Lithium is associated with oxidative stress and apoptosis, but the mechanism by which lithium protects against spinal cord injury remains poorly understood. In this study, we found that intraperitoneal administration of lithium chloride (LiCl) in a rat model of spinal cord injury alleviated pathological spinal cord injury and inhibited expression of tumor necrosis factor α, interleukin-6, and interleukin 1 ß. Lithium inhibited pyroptosis and reduced inflammation by inhibiting Caspase-1 expression, reducing the oxidative stress response, and inhibiting activation of the Nod-like receptor protein 3 inflammasome. We also investigated the neuroprotective effects of lithium intervention on oxygen/glucose-deprived PC12 cells. We found that lithium reduced inflammation, oxidative damage, apoptosis, and necrosis and up-regulated nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 in PC12 cells. All-trans retinoic acid, an Nrf2 inhibitor, reversed the effects of lithium. These results suggest that lithium exerts anti-inflammatory, anti-oxidant, and anti-pyroptotic effects through the Nrf2/heme oxygenase-1 pathway to promote recovery after spinal cord injury. This study was approved by the Animal Ethics Committee of Xi'an Jiaotong University (approval No. 2018-2053) on October 23, 2018.

[A case-control study of cervical spine Key-hole technique and anterior cervical Zero-P system in the treatment of cervical spondylotic radiculopathy].

OBJECTIVE: To explore the short-term clinical efficacy of single-stage cervical spondylotic radiculopathy (CSR) between the minimally invasive Key-hole technique and anterior cervical Zero profile intervertebral fusion system (Zero-P). METHODS: A retrospective analysis was performed on 45 patients who underwent surgical treatment for CSR from January 2017 to January 2020, including 21 in Key hole group (12 males and 9 females), followed up for 10-22(13.2±2.3) months;24 cases in Zero-P group (14 males and 10 females), and the follow up period was 10 to 23(12.7±1.9) months. Perioperative conditions (incision length, intraoperative blood loss, operation time, length of hospital stay, and complications) were compared between two groups, and X-rays of cervical spine before and after surgery and at the final follow-up were taken to analyzed curvature of the cervical spine, visual analogue scale(VAS) of pain before and after surgery, Oswestry Disability Index(ODI) and Japanese Orthopaedic Association (JOA) score of cervical spine were recorded to evaluate clinical efficacy. RESULTS: In Key-hole group and Zero-P group, the surgical incision length, intraoperative blood loss, operation time, final follow-up Cobb angle and immediate postoperative VAS score respectively were (1.2±0.2) cm, (5.3±0.3) cm;(35.3±9.7) ml, (120.2±13.5) ml;(56.4±11.3) min, (90.6±12.6) min;(3.2±3.9)°, (7.3±3.8)°;(2.8±1.2)points, (3.8±1.1) points;the Zero-P group was larger than the Key hole group, with statistical significance(P<0.05) . There were no statistically significant difference in length of hospital stay, ODI and JOA scores between two groups (P>0.05). After the follow-up, 1 case of neurostimulation symptoms in Key-hole group was relieved by conservative treatment, 2 cases improved after reoperation due to recurrence of cervical disc herniation;2 cases of neurostimulation symptoms in Zero-P group, 2 cases of throat discomfort, and 1 case dural tears were all relieved by conservative treatment. CONCLUSION: The cervical spine Key-hole technology is similar to the anterior cervical Zero-P system in the treatment of CSR. The Key-hole technique has certain advantages in incision length, intraoperative blood loss, and operation time. It is a safe, effective and can be widely used cervical spine surgery method.

Effects of ginsenoside Rb1 on spinal cord ischemia-reperfusion injury in rats.

BACKGROUND: The aim of this study was to evaluate the effects of different doses of ginsenoside Rb1 (GRb1) pretreatment on spinal cord ischemia-reperfusion (SCII) in rats and explore the potential mechanisms about the expression of survivin protein after the intervention. METHODS: A total of 90 healthy adult Sprague-Dawley (SD) rats were randomly divided into six groups: sham-operated (n = 15), SCII model (n = 15), and GRb1-treated groups (n = 60). The GRb1-treated group was divided into four subgroups: 10 mg/kg, 20 mg/kg, 40 mg/kg, and 80 mg/kg (n = 15). The corresponding dose of GRb1 was injected intraperitoneally 30 min before operation and every day after operation. Forty-eight hours after model establishment, the neurological function of hind limbs was measured with Basso, Beattie, and Bresnahan (BBB) scale. The superoxide dismutase (SOD) and malondialdehyde (MDA) levels in serum and spinal cord tissue were detected respectively. The expression of survivin protein was observed by immunofluorescence staining. HE and TUNEL staining were used to observe neural cell injury and apoptosis, respectively, in the spinal cord of rats with SCII. RESULTS: The intervention of different doses of GRb1 could increase SOD activity and decrease MDA content in serum and spinal cord tissue, increase survivin protein expression, and decrease neuronal apoptosis. It was dose-dependent, but there was no significant change between 40 mg/kg and 80 mg/kg. CONCLUSIONS: GRb1 could reduce the cell apoptosis induced by SCII through inhibiting oxidative stress. It can also inhibit apoptosis by promoting the expression of Survivin protein. Ginsenoside Rb1 had a dose-dependent protective effect on SCII in the dose range of 10 mg/kg-40 mg/kg.

Study of differential proteins in lung adenocarcinoma using laser capture microdissection combined with liquid chip-mass spectrometry technology.

BACKGROUND: In recent years the proportion of lung adenocarcinoma (adCA) which occurs in lung cancer patients has increased. Using laser capture microdissection (LCM) combined with liquid chip-mass spectrometry technology, we aimed to screen lung cancer biomarkers by studying the proteins in the tissues of adCA. METHODS: We used LCM and magnetic bead based weak cation exchange (MB-WCX) to separate and purify the homogeneous adCA cells and normal cells from six cases of fresh adCA and matched normal lung tissues. The proteins were analyzed and identified by matrix assisted laser desorption/ionization time-of-fight mass spectrometry (MALDI-OF-MS). We screened for the best pattern using a radial basic function neural network algorithm. RESULTS: About 2.895 × 10(6) and 1.584 × 10(6) cells were satisfactorily obtained by LCM from six cases of fresh lung adCA and matched normal lung tissues, respectively. The homogeneities of cell population were estimated to be over 95% as determined by microscopic visualization. Comparing the differentially expressed proteins between the lung adCA and the matched normal lung group, 221 and 239 protein peaks, respectively, were found in the mass-to-charge ration (M/Z) between 800 Da and 10 000 Da. According to t test, the expression of two protein peaks at 7521.5 M/Z and 5079.3 M/Z had the largest difference between tissues. They were more weakly expressed in the lung adCA compared to the matched normal group. The two protein peaks could accurately separate the lung adCA from the matched normal lung group by the sample distribution chart. A discriminatory pattern which can separate the lung adCA from the matched normal lung tissue consisting of three proteins at 3358.1 M/Z, 5079.3 M/Z and 7521.5 M/Z was established by a radial basic function neural network algorithm with a sensitivity of 100% and a specificity of 100%. CONCLUSIONS: Differential proteins in lung adCA were screened using LCM combined with liquid chip-mass spectrometry technology, and a biomarker model was established. It is possible that this technology is going to become a powerful tool in screening and early diagnosis of lung adCA.

[Changes of mitochondrial apoptosis in spinal cord ischemia-reperfusion injury and the effects of Herba Erigerontis Breviscapi Injection preconditioning intervention in rabbits].

OBJECTIVE: To investigate the mechanisms of mitochondrial apoptosis in spinal cord ischemia-reperfusion injury and the effects of Herba Erigerontis Breviscapi Injection preconditioning intervention. METHODS: Sixty Japanese rabbits were divided into sham-operated group, ischemia group, ischemia-reperfusion group (1, 6, 24 and 48 h), and Herba Erigerontis Breviscapi Injection group (1, 6, 24 and 48 h). Clamping the abdominal aorta was used to construct the rabbit model of spinal cord ischemia-reperfusion injury. The rabbits in the ischemia-reperfusion group and the Herba Erigerontis Breviscapi Injection group underwent reperfusion for 1, 6, 24, 48 h respectively after fifty-minute ischemia. The rabbits in the Herba Erigerontis Breviscapi Injection group were administered with Herba Erigerontis Breviscapi Injection at 9 mg/kg 30 minutes before ischemia. Rate of apoptotic cells was measured by flow cytometry; contents of caspase-9 and apoptosis-inducing factor (AIF) in cytoplasm and serum were measured by enzyme-linked immunosorbent assay. RESULTS: Compared with the sham-operated group and the ischemia group, the rates of apoptotic cells, the contents of caspase-9 and AIF in cytoplasm were increased at all time points after reperfusion, and the contents of caspase-9 and AIF in serum were decreased after 1 h and 6 h reperfusion, and increased after 24 h and 48 h reperfusion in the ischemia-reperfusion group. Herba Erigerontis Breviscapi Injection intervention could decrease the rate of apoptotic cells and the contents of caspase-9 and AIF in cytoplasm and serum as compared with those in the ischemia-reperfusion group, and the effects appeared after 1 h reperfusion. CONCLUSION: The apoptosis of nerve cells after spinal cord ischemia-reperfusion is related to the mitochondrial pathways. Herba Erigerontis Breviscapi Injection can inhibit nerve cell apoptosis by decreasing the contents of caspase-9 and AIF in cytoplasm and serum.